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1
Clerico, Aldo, Alberto Giannoni, Simona Vittorini, and Claudio Passino. "Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 1 (July 2011): H12—H20. http://dx.doi.org/10.1152/ajpheart.00226.2011.
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Thirty years ago, De Bold et al. ( 20 ) reported that atrial extracts contain some biologically active peptides, which promote a rapid and massive diuresis and natriuresis when injected in rats. It is now clear that the heart also exerts an endocrine function and in this way plays a key role in the regulation of cardiovascular and renal systems. The aim of this review is to discuss some recent insights and still-debated findings regarding the cardiac natriuretic hormones (CNHs) produced and secreted by cardiomyocytes (i.e., atrial natriuretic peptide and B-type natriuretic peptide). The functional status of the CNH system depends not only on the production/secretion of CNHs by cardiomyocytes but also on both the peripheral activation of circulating inactive precursor of natriuretic hormones and the transduction of the hormone signal by specific receptors. In this review, we will discuss the data supporting the hypothesis that the production and secretion of CNHs is the result of a complex integration among mechanical, chemical, hemodynamic, humoral, ischemic, and inflammatory inputs. The cross talk among endocrine function, adipose tissue, and sex steroid hormones will be discussed more in detail, considering the clinically relevant relationships linking together cardiovascular risk, sex, and body fat development and distribution. Finally, we will review the pathophysiological role and the clinical relevance of both peripheral maturation of the precursor of B-type natriuretic peptides and hormone signal transduction .
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Kellner, Michael, Ines Diehl, Kristina Knaudt, Cornelius Schüle, Holger Jahn, and Klaus Wiedemann. "C-type natriuretic peptide exerts stimulatory effects on the corticotropin-releasing hormone-induced secretion of hormones in normal man." European Journal of Endocrinology 136, no. 4 (April 1997): 388–93. http://dx.doi.org/10.1530/eje.0.1360388.
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Abstract C-type natriuretic peptide and atrial natriuretic peptide have been reported to bind to distinct receptors and to exert opposing effects on different systems. Although it is known that atrial natriuretic peptide inhibits the corticotropin-releasing hormone-stimulated hormone release in man, the corresponding action of C-type natriuretic peptide has so far not been characterized. We investigated the effects of 30-min infusions of 150 and 300 μg C-type natriuretic peptide on adrenocorticotropin, cortisol, and prolactin release stimulated by 100 μg corticotropin-releasing hormone and on cardiovascular parameters in 8 healthy male volunteers. Compared with placebo, 300 μg C-type natriuretic peptide significantly (P<0·05) enhanced the stimulation of cortisol (area under curve (arbitrary units): 520 ± 35 vs 651 ± 55) and prolactin (area under curve: 29 ± 3 vs 37 ± 5). Adrenocorticotropin levels were increased, but the differences did not reach statistical significance (maximum increment: 27±4 vs 36± 2 pg/ml). C-type natriuretic peptide at a dose of 150 μg had no clear effect on these hormones and C-type natriuretic peptide also produced no cardiovascular or subjective effects. Our data suggest stimulatory effects of C-type natriuretic peptide on corticotropinreleasing hormone-induced hormone release and offer further evidence for a complex role of different natriuretic peptides in endocrine regulation. European Journal of Endocrinology 136 388–393
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Charles, Christopher J., Miriam T. Rademaker, and A. Mark Richards. "Urocortin 1 modulates the neurohumoral response to acute nitroprusside-induced hypotension in sheep." Clinical Science 112, no. 9 (April 2, 2007): 485–91. http://dx.doi.org/10.1042/cs20060303.
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In addition to haemodynamic actions, Ucn1 (urocortin 1) has been reported to affect a number of hormonal systems; however, it remains unclear whether Ucn1 modulates circulating hormones under physiological conditions. Accordingly, in the present study, we have examined the effects of Ucn1 on haemodynamics, hormones and renal indices in normal conscious sheep subjected to a nitroprusside-induced hypotensive stimulus designed to alter hormonal levels within the physiological range. Ucn1 administration did not alter the haemodynamic response to nitroprusside-induced hypotension. However, compared with the rise observed on the control day, plasma ANP (atrial natriuretic peptide; P=0.043), BNP (brain natriuretic peptide; P=0.038) and endothelin-1 (P=0.011) levels were reduced following Ucn1 administration. Associated with this significant reduction in natriuretic peptides, the increase in urinary sodium output associated with rising pressures post-nitroprusside was abolished following Ucn1 administration (P=0.048). Ucn1 had no significant effect on the response of hormones of the renin–angiotensin–aldosterone system or the hypothalamo–pituitary–adrenal axis. In conclusion, Ucn1, administered at physiologically relevant levels during nitroprusside-induced hypotension, attenuates the secretion/release of endothelin-1 and the cardiac natriuretic peptides ANP and BNP. Suppression of ANP and BNP probably led to an attenuated natriuretic response to recovery from acute hypotension. The threshold for the action of Ucn1 on the natriuretic peptides and endothelin-1 appears to be below that of other actions of Ucn1.
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Saenger, Amy K., Daniel A. Dalenberg, Sandra C. Bryant, Stefan K. Grebe, and Allan S. Jaffe. "Pediatric Brain Natriuretic Peptide Concentrations Vary with Age and Sex and Appear to Be Modulated by Testosterone." Clinical Chemistry 55, no. 10 (October 1, 2009): 1869–75. http://dx.doi.org/10.1373/clinchem.2009.123778.
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Abstract Background: Natriuretic peptide concentrations in adults require age- and sex-specific reference intervals for optimal interpretation. Females have higher natriuretic peptide concentrations, and hypotheses suggest that estrogen may be responsible. This study sought to determine the influence of hormone modulation on N-terminal probrain natriuretic peptide (NT-proBNP) by using a pediatric cohort. Children/adolescents typically have rapid hormone changes during puberty, making them an ideal group to study. Methods: We selected 759 specimens (303 male, 456 female; ages 2 months to 18 years, mean 13 years) obtained from the Mayo Clinic Pediatric Residual Specimen Bank. We measured NT-proBNP, sex hormone–binding globulin (SHBG), estradiol, and testosterone by immunoassays or LC-MS/MS and calculated free testosterone. We performed univariate and multivariate analyses to investigate the significance of NT-proBNP with each hormone. Results: Reference values demonstrated a sex difference and sequential age differences in females. Univariate modeling of the hormones with NT-proBNP revealed an independent inverse association of NT-proBNP with testosterone, a direct association with SHBG, and no significant association with estradiol. Multivariate modeling confirmed a strong association of testosterone and SHBG with NT-proBNP. Correlation of hormones with NT-proBNP retained greater significance than either age or sex. Conclusions: In pediatric patients, NT-proBNP is independently associated with both testosterone and SHBG hormone concentrations. Measurements of testosterone are inversely associated with NT-proBNP, and estrogens are marginally associated with NT-proBNP in males but not females, suggesting that androgens and not estrogens modulate sex differences notable in natriuretic peptides. Children and adolescents may require an objective assessment of hormones if optimal interpretation of natriuretic peptide concentrations is desired or the concentrations are confounded. .
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MAFFEI, Silvia, Silvia DEL RY, Concetta PRONTERA, and Aldo CLERICO. "Increase in circulating levels of cardiac natriuretic peptides after hormone replacement therapy in postmenopausal women." Clinical Science 101, no. 5 (September 21, 2001): 447–53. http://dx.doi.org/10.1042/cs1010447.
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The mechanisms that mediate the cardioprotective action of steroid hormones in postmenopausal women are poorly understood. To study the inter-relationship between female steroid hormones and cardiac natriuretic peptides, plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were measured in postmenopausal women, both before and after oestrogen replacement therapy. A total of 22 healthy postmenopausal women (mean age 51.9±4.6 years) were enrolled in the study; all had been postmenopausal for at least 1 year and all reported climacteric symptoms accompanied by increased levels of follicle-stimulating hormone (>30m-i.u./ml) and luteinizing hormone (>20m-i.u./ml), and a reduction in oestradiol (<25pg/ml). All women were given hormone replacement therapy with transdermal oestradiol, either patch (50μg/24 h) or gel (1mg/day), cyclically combined with oral dihydrogesterone (10mg/day for 12 days/month, on days 19-30 of the month). ANP and BNP were measured directly in plasma samples with specific and sensitive immunoradiometric assays before and after hormone replacement therapy (transdermal oestradiol combined with oral dihydrogesterone). Body weight, arterial blood pressure and echocardiographic examination values did not change after hormone replacement therapy. As expected, serum oestradiol increased significantly and gonadotropins decreased as an effect of the hormone replacement therapy. On average, both ANP and BNP had increased significantly after 3 months of hormone replacement therapy [ANP: before treatment, 17.6±9.6pg/ml; after, 23.6±5.6pg/ml (P = 0.0173); BNP: before treatment, 12.6±10.2pg/ml; after, 19.8±14.0pg/ml (P<0.0001)]. Our study indicates that hormone replacement therapy for a period of 3 months induces a rise in the circulating levels of cardiac natriuretic hormones in postmenopausal women. Our data also suggest the working hypothesis that cardiac natriuretic peptides may play an important role in mediating the cardioprotective effects of female steroid sex hormones in women throughout life.
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Rademaker, Miriam Tessa, Christopher John Charles, Eric Arnold Espiner, Michael Gary Nicholls, Arthur Mark Richards, and Teddy Kosoglou. "Neutral Endopeptidase Inhibition: Augmented Atrial and Brain Natriuretic Peptide, Haemodynamic and Natriuretic Responses in Ovine Heart Failure." Clinical Science 91, no. 3 (September 1, 1996): 283–91. http://dx.doi.org/10.1042/cs0910283.
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1. Atrial and brain natriuretic peptide are both circulating hormones subject to degradation by neutral endopeptidase 24.11. Whereas endogenous levels of atrial natriuretic peptide are increased by neutral endopeptidase inhibition in most pathophysiological states, the effect on brain natriuretic peptide and the influence of cardiac status is less clear. To further evaluate the role of neutral endopeptidase 24.11, we directly compared the responses of atrial and brain natriuretic peptide, together with the effects on other vasoactive hormones, haemodynamics and renal indices, to a neutral endopeptidase inhibitor, SCH32615, and a vehicle control in eight conscious sheep before and during pacing-induced heart failure. 2. In normal animals, SCH32615 significantly increased concentrations of plasma atrial natriuretic peptide (22±5 pmol/l compared with 14±2 pmol/l in control, 1.6-fold increase) and brain natriuretic peptide (6.5±1.2 pmol/l compared with 4.1±0.7 pmol/l in control, 1.6-fold increase), whereas in heart failure, plasma levels of atrial natriuretic peptide (306±38 pmol/l compared with 187±25 pmol/l in control, 1.6-fold increase) and brain natriuretic peptide (93±11 pmol/l compared with 55 ± 9 pmol/l in control, 1.7-fold increase) were elevated to a significantly greater absolute, but proportionately similar, extent. In both normal and heart-failed animals, SCH32615 induced reductions in mean arterial pressure and left atrial pressure and increases in haematocrit, plasma cGMP and endogenous creatinine clearance. However, only in heart failure did neutral endopeptidase inhibition induce a significant and marked natriuresis (> 10-fold increase) and diuresis (4-fold increase), together with suppression of renin activity and haemodynamic effects including decreased peripheral resistance and raised cardiac output. 3. In conclusion, neutral endopeptidase inhibition increases plasma concentrations of atrial and brain natriuretic peptide to a proportionately similar extent in both normal and heart-failed sheep. The striking natriuresis and diuresis and additional haemodynamic effects demonstrated in sheep with heart failure, where natriuretic peptide levels are elevated compared with normal sheep, supports the concept that neutral endopeptidase inhibition augments endogenous atrial and brain natriuretic peptide.
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Saba, Sabiha R., Amanda H. Garces, Linda C. Clark, John Soto, William R. Gower, and David L. Vesely. "Immunocytochemical Localization of Atrial Natriuretic Peptide, Vessel Dilator, Long-acting Natriuretic Peptide, and Kaliuretic Peptide in Human Pancreatic Adenocarcinomas." Journal of Histochemistry & Cytochemistry 53, no. 8 (August 2005): 989–95. http://dx.doi.org/10.1369/jhc.4a6572.2005.
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We recently found that four peptide hormones synthesized by the same gene completely inhibit the growth of human pancreatic adenocarcinomas in athymic mice. The present immunocytochemical investigation was designed to determine where in the adenocarcinomas these peptide hormones localize. Atrial natriuretic peptide, vessel dilator, long-acting natriuretic peptide, and kaliuretic peptide localized to the cytoplasm and nucleus of the human pancreatic adenocarcinomas, which is consistent with their ability to decrease DNA synthesis in the nucleus of this cancer. In this first investigation of where these peptide hormones with anticancer effects localize in any cancer, these peptide hormones also localized to the endothelium of capillaries and fibroblasts within these cancers. This is the first demonstration of growth-inhibiting peptide hormones localizing to the nucleus, where they inhibit DNA synthesis and may interact with growth-promoting hormones that localize there as the etiology of their ability to inhibit the growth of adenocarcinomas both in vitro and in vivo.
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Clerico, Aldo, Silvia Del Ry, and Daniela Giannessi. "Measurement of Cardiac Natriuretic Hormones (Atrial Natriuretic Peptide, Brain Natriuretic Peptide, and Related Peptides) in Clinical Practice: The Need for a New Generation of Immunoassay Methods." Clinical Chemistry 46, no. 10 (October 1, 2000): 1529–34. http://dx.doi.org/10.1093/clinchem/46.10.1529.
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Abstract Background: Cardiac natriuretic hormones (CNHs) are a family of related peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and other peptides derived from the N-terminal portion of the proANP and proBNP peptide chains. Assays for cardiac natriuretic peptides have been proposed to help assess clinical conditions associated with expanded fluid volume. In particular, the assays can be useful for distinguishing healthy subjects from patients in different stages of heart failure. Measurements of these hormones have also been considered for prognostic indicators of long-term survival in patients with heart failure and/or after acute myocardial infarction. The different CNHs differ in their production/secretion patterns and have different clearance rates. Furthermore, there are numerous proposed assay configurations for each of these hormones, and it is not clear which assay provides the best pathophysiological and/or clinical information. Approach: Here we review recent studies concerning the competitive (such as RIA, enzyme immunoassay, or luminescence immunoassay) and noncompetitive immunoassays (such as two-site IRMA, ELISA, or immunoluminometric assay) for the different cardiac natriuretic peptides to compare the analytical characteristics and clinical relevance of assays for the different CNHs and the different assay formats. Content: Developing sensitive, precise, and accurate immunoassays for cardiac natriuretic peptides has been difficult because of their low concentrations (on average, ∼3–6 pmol/L) in healthy subjects and because of their structural, metabolic, and physiological characteristics. Competitive assays have historically suffered from lack of sensitivity and specificity for the biologically active peptides. These usually require tedious extraction procedures prior to analysis. Recently, immunometric assays have been developed that have improved sensitivity and specificity; it appears these will be the methods of choice. Summary: To date, there is no consensus on the best assay procedure of cardiac natriuretic peptides. To facilitate widespread propagation of determination of these hormones in routine clinical practice, it will be necessary to study the new generation of noncompetitive immunometric methods that are less time-consuming and more sensitive and specific. Although several studies suggest that BNP exhibits better clinical utility than the other CNHs, more studies examining multiple CNHs in the same cohorts of patients will be necessary.
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Charles, C. J., E. A. Espiner, A. M. Richards, M. G. Nicholls, and T. G. Yandle. "Comparative bioactivity of atrial, brain, and C-type natriuretic peptides in conscious sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 6 (June 1, 1996): R1324—R1331. http://dx.doi.org/10.1152/ajpregu.1996.270.6.r1324.
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Although atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) appear to share functional homology, there is doubt concerning a possible endocrine function for C-type natriuretic peptide (CNP) and the relative potency of species-specific forms of these hormones. Accordingly, we have examined the biological effects, interactions, and pharmacokinetics of equimolar doses (0.5 followed by 2.5 pmol.kg-1.min-1, each for 2 h) of species-specific forms of ANP, BNP-26, and CNP-22 in vehicle-controlled studies in normal conscious sheep. Although pharmacokinetics (metabolic clearance rates of 5.7 +/- 1.17, 7.5 +/- 1.36, and 4.7 +/- 0.71 l/min and half-lives of 3.9 +/- 0.42, 2.5 +/- 0.21, and 2.0 +/- 0.18 min for ANP, BNP, and CNP, respectively) are similar, the biological effects and actions on endogenous natriuretic peptide levels differ. Plasma BNP was significantly increased by CNP infusion (P < 0.0001), as was CNP by BNP infusions (P = 0.0009). Compared with ANP and BNP, which were equipotent in stimulating plasma guanosine 3',5'-cyclic monophosphate (cGMP; P < 0.0001 for both) and lowering arterial pressure (P < 0.05 for both) and cardiac output, CNP infusions induced only a small increment in cGMP and had no significant hemodynamic actions. In contrast, all three peptides suppressed plasma aldosterone levels (P < 0.05 for each), yet none induced significant natriuresis. Actions of CNP to increase BNP (and ANP) may account for the observed bioactivity of CNP. The findings show that potentially important interactions occur among all three hormones that need to be considered when interpreting the effects of individual peptides, particularly CNP.
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Munger, K. A., M. Sugiura, K. Takahashi, T. Inagami, and K. F. Badr. "A role for atrial natriuretic peptide in endothelin-induced natriuresis." Journal of the American Society of Nephrology 1, no. 12 (June 1991): 1278–83. http://dx.doi.org/10.1681/asn.v1121278.
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Systemic administration of low-dose endothelin increases urinary sodium excretion rate despite mild to moderate reductions in renal plasma flow and glomerular filtration rates. The role of atrial natriuretic peptide in endothelin-induced natriuresis was investigated. Administration of 2.50 pmol/min of endothelin to euvolemic rats resulted in increases in plasma atrial natriuretic peptide levels from 127 +/- 18 to 169 +/- 23 pg/mL. However, a lower dose of endothelin (0.63 pmol/min) or saline did not increase plasma levels of atrial natriuretic peptide. Mean arterial pressure was unchanged at the lower dose of endothelin and increased only slightly in rats receiving 2.5 pmol/min. To assess functional significance, renal responses to endothelin (2.5 pmol/min) in the absence and presence of a specific anti-rat atrial natriuretic peptide antibody were compared. Equivalent reductions in renal blood flow were observed. Urinary sodium excretion rates increased significantly in non-ANP-antibody-treated rats by 33 +/- 7 and 82 +/- 20% at 10 and 30 min, respectively. Atrial natriuretic peptide antibody blunted markedly endothelin-induced natriuresis: urinary sodium excretion rates changed insignificantly by 18 +/- 10 and 30 +/- 14%, respectively. Thus, endothelin infusion results in increases in plasma atrial natriuretic peptide levels, which may contribute to endothelin-induced natriuresis, providing evidence for potentially significant interactions between these peptide hormones in the regulation of sodium balance and renal vascular tone.
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Vesely, D. L., S. Chiou, M. A. Douglass, M. T. McCormick, G. Rodriguez-Paz, and D. D. Schocken. "Kaliuretic peptide and long acting natriuretic peptide as well as atrial natriuretic factor inhibit aldosterone secretion." Journal of Endocrinology 146, no. 3 (September 1995): 373–80. http://dx.doi.org/10.1677/joe.0.1460373.
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Abstract The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1–30 (long acting natriuretic peptide), 31–67 (vessel dilator) and 79–98 (kaliuretic peptide) as well as 99–126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P<0·001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P<0·01) decreased plasma aldosterone levels which remained significantly (P<0·001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P<0·01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P<0·001) than following ANF infusion. Journal of Endocrinology (1995) 146, 373–380
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Potter, Lincoln R., Sarah Abbey-Hosch, and Deborah M. Dickey. "Natriuretic Peptides, Their Receptors, and Cyclic Guanosine Monophosphate-Dependent Signaling Functions." Endocrine Reviews 27, no. 1 (November 16, 2005): 47–72. http://dx.doi.org/10.1210/er.2005-0014.
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Natriuretic peptides are a family of structurally related but genetically distinct hormones/paracrine factors that regulate blood volume, blood pressure, ventricular hypertrophy, pulmonary hypertension, fat metabolism, and long bone growth. The mammalian members are atrial natriuretic peptide, B-type natriuretic peptide, C-type natriuretic peptide, and possibly osteocrin/musclin. Three single membrane-spanning natriuretic peptide receptors (NPRs) have been identified. Two, NPR-A/GC-A/NPR1 and NPR-B/GC-B/NPR2, are transmembrane guanylyl cyclases, enzymes that catalyze the synthesis of cGMP. One, NPR-C/NPR3, lacks intrinsic enzymatic activity and controls the local concentrations of natriuretic peptides through constitutive receptor-mediated internalization and degradation. Single allele-inactivating mutations in the promoter of human NPR-A are associated with hypertension and heart failure, whereas homozygous inactivating mutations in human NPR-B cause a form of short-limbed dwarfism known as acromesomelic dysplasia type Maroteaux. The physiological effects of natriuretic peptides are elicited through three classes of cGMP binding proteins: cGMP-dependent protein kinases, cGMP-regulated phosphodiesterases, and cyclic nucleotide-gated ion channels. In this comprehensive review, the structure, function, regulation, and biological consequences of natriuretic peptides and their associated signaling proteins are described.
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Vesely, David L. "Natriuretic peptides and acute renal failure." American Journal of Physiology-Renal Physiology 285, no. 2 (August 2003): F167—F177. http://dx.doi.org/10.1152/ajprenal.00259.2002.
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Atrial natriuretic peptides (ANPs) are a family of peptide hormones, e.g., ANP, long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide synthesized by the ANP gene. Brain natriuretic peptide (BNP) and C-type natriuretic peptide are also members of this family but are synthesized by separate genes. Within the kidney, the ANP prohormone's posttranslational processing is different from that of other tissues, resulting in an additional four amino acids added to the NH2terminus of ANP (e.g., urodilatin). Each of these natriuretic and diuretic peptides increases within the circulation with acute renal failure (ARF). Renal transplantation but not hemodialysis returns their circulating concentrations to those of healthy individuals. BNP and adrenomedullin, a 52-amino acid natriuretic peptide, have beneficial effects on glomerular hypertrophy and glomerular injury but do not improve tubular injury (i.e., acute tubular necrosis). Vessel dilator ameliorates acute tubular necrosis with regeneration of the brush borders of proximal tubules. Vessel dilator decreases mortality in ARF from 88 to 14% at day 6 of ARF, even when given 2 days after renal failure has been established.
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Fonteles, Manassés Claudino, and Nilberto Robson Falcão do Nascimento. "Guanylin peptide family: history, interactions with ANP, and new pharmacological perspectives." Canadian Journal of Physiology and Pharmacology 89, no. 8 (August 2011): 575–85. http://dx.doi.org/10.1139/y11-050.
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The guanylin family of peptides has 3 subclasses of peptides containing either 3 intramolecular disulfide bonds found in bacterial heat-stable enterotoxins (ST), or 2 disulfides observed in guanylin and uroguanylin, or a single disulfide exemplified by lymphoguanylin. These peptides bind to and activate cell-surface receptors that have intrinsic guanylate cyclase (GC) activity. These hormones are synthesized in the intestine and released both luminally and into the circulation, and are also produced within the kidney. Stimulation of renal target cells by guanylin peptides in vivo or ex vivo elicits a long-lived diuresis, natriuresis, and kaliuresis by both cGMP-dependent and independent mechanisms. Uroguanylin may act as a hormone in a novel endocrine axis linking the digestive system and kidney as well as a paracrine system intrarenally to increase sodium excretion in the postprandial period. This highly integrated and redundant mechanism allows the organism to maintain sodium balance by eliminating excess sodium in the urine. In addition, small concentrations of the atrial natriuretic peptide (ANP) can synergize with low concentrations of both guanylin or uroguanylin, which do not induce natriuresis per se, to promote significant natriuresis. Interestingly, the activation of the particulate guanylate cyclase receptors by natriuretic peptides can promote relaxation of animal and human penile erectile tissue and increase intracavernosal pressure to induce penile erection. These peptides can be prototypes for new drugs to treat erectile dysfunction, especially in patients with endothelial and nitrergic dysfunction, such as in diabetes.
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Rosenzweig, Anthony, and Christine E. Seidman. "Atrial Natriuretic Factor and Related Peptide Hormones." Annual Review of Biochemistry 60, no. 1 (June 1991): 229–55. http://dx.doi.org/10.1146/annurev.bi.60.070191.001305.
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Patel, Jeetendra B., Maria L. Valencik, Allison M. Pritchett, John C. Burnett, John A. McDonald, and Margaret M. Redfield. "Cardiac-specific attenuation of natriuretic peptide A receptor activity accentuates adverse cardiac remodeling and mortality in response to pressure overload." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 2 (August 2005): H777—H784. http://dx.doi.org/10.1152/ajpheart.00117.2005.
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Atrial (ANP) and brain (BNP) natriuretic peptides are hormones of myocardial cell origin. These hormones bind to the natriuretic peptide A receptor (NPRA) throughout the body, stimulating cGMP production and playing a key role in blood pressure control. Because NPRA receptors are present on cardiomyocytes, we hypothesized that natriuretic peptides may have direct autocrine or paracrine effects on cardiomyocytes or adjacent cardiac cells. Because both natriuretic peptides and NPRA gene expression are upregulated in states of pressure overload, we speculated that the effects of the natriuretic peptides on cardiac structure and function would be most apparent after pressure overload. To attenuate cardiomyocyte NPRA activity, transgenic mice with cardiac specific expression of a dominant-negative (DN-NPRA) mutation (HCAT D 893A) in the NPRA receptor were created. Cardiac structure and function were assessed (avertin anesthesia) in the absence and presence of pressure overload produced by suprarenal aortic banding. In the absence of pressure overload, basal and BNP-stimulated guanylyl cyclase activity assessed in cardiac membrane fractions was reduced. However, systolic blood pressure, myocardial cGMP, log plasma ANP levels, and ventricular structure and function were similar in wild-type (WT-NPRA) and DN-NPRA mice. In the presence of pressure overload, myocardial cGMP levels were reduced, and ventricular hypertrophy, fibrosis, filling pressures, and mortality were increased in DN-NPRA compared with WT-NPRA mice. In addition to their hormonal effects, endogenous natriuretic peptides exert physiologically relevant autocrine and paracrine effects via cardiomyocyte NPRA receptors to modulate cardiac hypertrophy and fibrosis in response to pressure overload.
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Szabó, Gábor, János Rigó jr., and Bálint Nagy. "Physiology and clinical importance of the natriuretic peptide system." Orvosi Hetilap 152, no. 26 (June 2011): 1025–34. http://dx.doi.org/10.1556/oh.2011.29153.
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In the last three decades many members of the natriuretic peptide family was isolated. The function and physiological role of these peptides are pleiotropic. All natriuretic peptides are synthesized from polypeptide precursors. Together with the sympathetic nervous system and other hormones they play key roles, like an endogenous system in the regulation of the body fluid homeostasis and blood pressure. Changes in this balance lead to dysfunction in the endothel and left ventricle, which can cause severe complications. In many cardiovascular diseases natriuretic peptides serve not only as marker for diagnosis and prognosis but they have therapeutic importance. In the last years the potential use of the elevated BNP levels for diagnosis of pre-eclampsia was examined. In our review we discuss the current understanding of molecular biology, biochemistry and clinical relevance of natriuretic peptides. Orv. Hetil., 2011, 152, 1025–1034.
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Tanase, Daniela Maria, Smaranda Radu, Sinziana Al Shurbaji, Genoveva Livia Baroi, Claudia Florida Costea, Mihaela Dana Turliuc, Anca Ouatu, and Mariana Floria. "Natriuretic Peptides in Heart Failure with Preserved Left Ventricular Ejection Fraction: From Molecular Evidences to Clinical Implications." International Journal of Molecular Sciences 20, no. 11 (May 28, 2019): 2629. http://dx.doi.org/10.3390/ijms20112629.
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The incidence of heart failure with preserved ejection fraction (HFpEF) is increasing and its challenging diagnosis and management combines clinical, imagistic and biological data. Natriuretic peptides (NPs) are hormones secreted in response to myocardial stretch that, by increasing cyclic guanosine monophosphate (cGMP), counteract myocardial fibrosis and hypertrophy, increase natriuresis and determine vasodilatation. While their role in HFpEF is controversial, most authors focused on b-type natriuretic peptides (BNPs) and agreed that patients may show lower levels. In this setting, newer molecules with an increased specificity, such as middle-region pro-atrial natriuretic peptide (MR-proANP), emerged as promising markers. Augmenting NP levels, either by NP analogs or breakdown inhibition, could offer a new therapeutic target in HFpEF (already approved in their reduced EF counterparts) by increasing the deficient cGMP levels found in patients. Importantly, these peptides also retain their prognostic value. This narrative review focuses on NPs’ physiology, diagnosis, therapeutic and prognostic implication in HFpEF.
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Ogawa, Tsuneo, and Adolfo J. de Bold. "The heart as an endocrine organ." Endocrine Connections 3, no. 2 (June 2014): R31—R44. http://dx.doi.org/10.1530/ec-14-0012.
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The concept of the heart as an endocrine organ arises from the observation that the atrial cardiomyocytes in the mammalian heart display a phenotype that is partly that of endocrine cells. Investigations carried out between 1971 and 1983 characterised, by virtue of its natriuretic properties, a polypeptide referred to atrial natriuretic factor (ANF). Another polypeptide isolated from brain in 1988, brain natriuretic peptide (BNP), was subsequently characterised as a second hormone produced by the mammalian heart atria. These peptides were associated with the maintenance of extracellular fluid volume and blood pressure. Later work demonstrated a plethora of other properties for ANF and BNP, now designated cardiac natriuretic peptides (cNPs). In addition to the cNPs, other polypeptide hormones are expressed in the heart that likely act upon the myocardium in a paracrine or autocrine fashion. These include the C-type natriuretic peptide, adrenomedullin, proadrenomedullin N-terminal peptide and endothelin-1. Expression and secretion of ANF and BNP are increased in various cardiovascular pathologies and their levels in blood are used in the diagnosis and prognosis of cardiovascular disease. In addition, therapeutic uses for these peptides or related substances have been found. In all, the discovery of the endocrine heart provided a shift from the classical functional paradigm of the heart that regarded this organ solely as a blood pump to one that regards this organ as self-regulating its workload humorally and that also influences the function of several other organs that control cardiovascular function.
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Lyall, Fiona, and J. J. Morton. "Specific binding of atrial natriuretic peptide to rat mesenteric artery: Effect of calcium and 5-guanylylimidodiphosphate." Clinical Science 73, no. 6 (December 1, 1987): 573–79. http://dx.doi.org/10.1042/cs0730573.
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1. High-dissociation equilibrium constant (20 pmol/l, receptor number 17 fmol/mg) and low-dissociation equilibrium constant (10 nmol/l, receptor number 5 nmol/mg) affinity binding sites for atrial natriuretic peptide have been identified in membrane preparations from rat mesenteric artery. 2. Tracer degradation was corrected for mathematically and binding data were analysed by a non-linear computer technique. 3. Non-atrial natriuretic peptide vasoactive hormones, angiotensin II, vasopressin and bradykinin, did not compete for the high-affinity site. Related peptides with either C- or N-terminal amino acids missing still competed, while peptides without an intact disulphide bridge did not compete. 4. Neither the addition nor the removal of calcium affected the affinity or density of binding sites. Also the non-hydrolysable guanosine triphosphate analogue 5-guanylylimidodiphosphate had no effect on either affinity or number of sites. 5. These results indicate the presence of a specific high-affinity vascular receptor for atrial natriuretic peptide which could interact with the hormone under physiological conditions. The mechanism of binding is uncertain but is unlikely to involve calcium- or guanosine triphosphate-associated regulatory sites.
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Oxley, K., and J. Baxter. "B-type natriuretic peptide: use and misuse in the older patient." Reviews in Clinical Gerontology 22, no. 3 (May 9, 2012): 179–83. http://dx.doi.org/10.1017/s0959259812000068.
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SummaryB-type natriuretic peptide (BNP) and the inactive N-terminal fragment of the precursor (NT-proBNP) are hormones predominantly produced by the cardiac myocyte. It has been shown that very high levels of circulating natriuretic peptides correlate with a diagnosis of heart failure. In view of this, the current NICE, SIGN and European Society of Cardiology guidelines on heart failure recommend the measurement of natriuretic peptides as part of the diagnostic pathway for patients with suspected heart failure in primary care. Patients should be stratified according to results, with high-risk patients referred and reviewed by specialist services within 2 weeks. There has also been interest regarding the potential use of natriuretic peptides in disease surveillance, therapeutic monitoring and in-patient discharge planning. Consequently, it is a test that we will encounter with increasing frequency in clinical practice.Heart failure is common in older people, hence geriatricians need to have an understanding of the implications of natriuretic peptide levels. The test can be affected by both physiological and pharmacological factors and this should be taken into consideration when interpreting results.
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Wilkins, M. R., D. J. Nunez, and J. Wharton. "The natriuretic peptide family: turning hormones into drugs." Journal of Endocrinology 137, no. 3 (June 1993): 347–59. http://dx.doi.org/10.1677/joe.0.1370347.
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Zhao, Z., and L. Ma. "Regulation of axonal development by natriuretic peptide hormones." Proceedings of the National Academy of Sciences 106, no. 42 (October 1, 2009): 18016–21. http://dx.doi.org/10.1073/pnas.0906880106.
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Hamada, Mareomi, Yuji Shigematsu, Hideo Kawakami, Naoto Minamino, Kenji Kangawa, Hisayuki Matsuo, and Kunio Hiwada. "Increased Plasma Levels of Adrenomedullin in Patients with Hypertrophic Cardiomyopathy: Its Relation to Endothelin-1, Natriuretic Peptides and Noradrenaline." Clinical Science 94, no. 1 (January 1, 1998): 21–28. http://dx.doi.org/10.1042/cs0940021.
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1. The aim of this study was to elucidate the pathophysiological role of adrenomedullin and the relation between adrenomedullin and other hormones in patients with hypertrophic cardiomyopathy. 2. Fourteen patients with hypertrophic obstructive cardiomyopathy (HOCM), 26 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) and 14 normal control subjects participated in this study. Radioimmunoassay for plasma adrenomedullin concentration was performed with adrenomedullin-M antibody. Plasma levels of endothelin-1, atrial and brain natriuretic peptides and noradrenaline were also measured. 3. Plasma levels of adrenomedullin were higher in patients with hypertrophic cardiomyopathy (8.43 ± 3.73 pmol/l) than in normal controls (5.24 ± 0.44 pmol/l, P < 0.005). There was no significant difference between HOCM and HNCM patients. There was a weak correlation between plasma levels of adrenomedullin and total 12-lead QRS voltage in patients with hypertrophic cardiomyopathy (r = 0323, P < 0.05) 4. Plasma levels of endothelin-1, atrial and brain natriuretic peptides were higher in hypertrophic cardiomyopathy than in normal controls. Endothelin-1 showed no significant difference between HOCM and HNCM patients, but atrial and brain natriuretic peptides were higher in HOCM than in HNCM patients. There was a positive correlation between plasma levels of adrenomedullin and endothelin-1 (r = 0.575, P < 0.0001), but no correlation between plasma levels of adrenomedullin and atrial natriuretic peptide, brain natriuretic peptide and noradrenaline. 5. Our results indicate that adrenomedullin may play an important role to maintain haemodynamics in patients with hypertrophic cardiomyopathy, and its action may be related to endothelin-1 but independent of atrial natriuretic peptide, brain natriuretic peptide and noradrenaline.
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Walther, T., and H. Stepan. "C-type natriuretic peptide in reproduction, pregnancy and fetal development." Journal of Endocrinology 180, no. 1 (January 1, 2004): 17–22. http://dx.doi.org/10.1677/joe.0.1800017.
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C-type natriuretic peptide (CNP) belongs to the natriuretic peptide family that consists of three structurally related peptides with a 17-amino acid ring linked by a disulfide bond. In contrast to atrial and brain natriuretic peptides that are mainly cardiovascular hormones, CNP acts predominantly in an autocrine/paracrine fashion, is commonly considered to be an endothelial hormone with antimitogenic properties, and is characterized as a regulator of endochondral ossification. Its biological effects are mediated by an intracellular cGMP accumulation via specific membrane-bound guanylyl cyclase B (GC-B) activation. There is growing evidence that this peptide is also involved in various reproductive processes as well as in embryonic and fetal development. In rodents, CNP and its receptor are highly expressed in the uterus and ovaries with specific regulation during the estrous cycle. During pregnancy, CNP mRNA is detectable in mice embryos and shows an organ-specific expression in maternal reproductive tIssues with the highest concentration in the placenta. This could indicate a defined biological function of the CNP/GC-B/cGMP axis in gestation e.g. antagonizing vasoconstrictive peptides like angiotensin II. In humans, besides a postulated fetal de novo synthesis of CNP, both the peptide and its receptor are expressed in the placenta and myometrium with opposite regulation of CNP in pregnancies complicated by pre-eclampsia or intrauterine growth retardation. Since the maternal plasma levels do not reflect these alterations, one can conclude that this part of the natriuretic peptide system acts locally suggesting that CNP-stimulated cGMP release exhibits organ-specific effects. Importantly, CNP has also become a peptide with a distinct role in male reproductive processes, since endocrine function of the testis and the regulation of penile erection are regulated by the CNP/GC-B axis. This review gives a comprehensive overview of the multiple functions of CNP in reproduction and pregnancy as well as in embryonic and fetal development.
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Dajak, Marijana, Svetlana Ignjatovic, and Nada Majkic-Singh. "The significance of determination of heart natriuretic peptides in heart insufficiency." Jugoslovenska medicinska biohemija 22, no. 4 (2003): 311–17. http://dx.doi.org/10.2298/jmh0304311d.
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Heart natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act as key regulators of homeostasis of body fluids volume and blood pressure, by decreasing salt excess and water retention, and by inhibiting intensive action of sympathetic nervous system and secretion of vasoconstrictor hormones. Plasma ANP, N-terminal pro-atrial natriuretic peptide (NT-proANP), BNP and N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations are considerably increased in heart insufficiency. Intracardiac pressure and atrial and ventricular wall tension are the prime regulators of natriuretic peptides release from the heart. ANP primarily reflects atrial, and BNP ventricular overload. The in vitro stabilities of NT-proANP, BNP and NT-proBNP in EDTA whole blood are sufficient for routine determination. Specific immunochemical tests with acceptable precision are commercially available. However, the determinations are not standardized, which makes difficulties during the comparation of results gained by tests from different manufactures. BNP and NT-proBNP are in relation to ANP and NT-proANP, better diagnostic and prognostic markers of heart insufficiency. BNP measurement is useful for screening in high-risk population. BNP has an excellent negative predictive value for left ventricular dysfunction. It is also suitable for screening hypertensive patients for the discovery of hypertrophy or/and dysfunction of left ventriculy, as well as for risk assessment during the subacute phase of acute myocardial infarction. BNP and NT-proBNP measurement is also useful for treatment guidance and optimization of therapy in heart insufficiency. However, BNP determination cannot replace echocardiography or similar techniques, because these methods provide different information. Thus for the cardiologists natriuretic peptides determination is useful addition to the standard clinical investigation of patients with ventricular dysfunction.
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Kondratieva, E. A., N. V. Dryagina, M. I. Aybazova, S. A. Kondratiev, A. A. Denisova, N. E. Ivanova, M. I. Yarmolinskaya, and A. N. Kondratiev. "Prognosis of prolonged disorders of consciousness outcome based on the determination of certain hormones and natriuretic peptide." Messenger of ANESTHESIOLOGY AND RESUSCITATION 16, no. 6 (January 27, 2020): 16–22. http://dx.doi.org/10.21292/2078-5658-2019-16-6-16-22.
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Introduction: Changes in hormonal status in patients with prolonged disorders of consciousness (PDC) remain poorly understood. There are no studies devoted to the investigation of prognostic value of hormonal changes to predict the outcome which is primarily due to a relatively small number of patients, different variants of structural brain disorders in vegetative state (VS) patients, concomitant somatic pathology including typical complications.The objective: to study the correlation between outcomes in VS patients with hormonal status and the level of natriuretic peptide. Subjects and methods. 275 patients in VS were examined for the time period from 2007 to 2017. 152 patients had sequela of traumatic brain injury (TBI) and 123 patients suffered from hypoxic brain damage. All patients matched the international criteria of VS diagnosis. In all patients, blood samples were collected during the first week after admission to ICU to test hormones and natriuretic peptide levels. ACTH, cortisol, TSH, free T3 and T4 , STH, prolactin and natriuretic peptide were tested in the period from 2 to 4 months of staying in VS. In men, the level of total testosterone, LH and FSH was additionally tested. The obtained data were compared with VS outcome.Results. The tested hormones were stably insufficient only in few VS patients. None of the tested hormones of the hypothalamic-pituitary-adrenal axis made a reliable criterion for predicting VS outcome. The tendency of disrupted rhythm of cortisol secretion was found to be most frequent and consistent, with higher rates in the evening hours. The average value of STH was higher in men with sequela of traumatic brain injury who had recovered consciousness versus those who remained in VS. A significant decrease in testosterone levels, regardless of age, was found in the patients with TBI sequela. Mean levels of LH were higher in patients with TBI sequela and hypoxia who remained unconscious versus patients who later restored consciousness. The average level of FSH was higher in patients who had recovered consciousness compared to those who remained in chronic VS. The increased level of natriuretic peptide was observed both in patients who remained in chronic VS and in those who restored consciousness.Conclusions. When investigating levels of certain hormones, no specific endocrine background characterizing this category of patients was found. Abnormal rhythms of some hormones secretion, in particular cortisol, can be considered typical of VS patients especially patients with TBI sequela.
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Richards, A. M., G. Tonolo, R. Fraser, J. J. Morton, B. J. Leckie, S. G. Ball, and J. I. S. Robertson. "Diurnal change in plasma atrial natriuretic peptide concentrations." Clinical Science 73, no. 5 (November 1, 1987): 489–95. http://dx.doi.org/10.1042/cs0730489.
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1. Diurnal changes in plasma concentrations of atrial natriuretic peptide (ANP), renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were investigated in seven normal volunteers studied under standardized conditions of dietary sodium, posture and physical activity. After completion of the diurnal study serial measurements of these variables were continued during, and on recovery from, a 2 day period of severe sodium depletion. 2. Clear diurnal variations in plasma concentrations of renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were observed. 3. Plasma ANP concentrations also varied significantly over 24 h. Values peaked about mid-day and a distinct trough in peptide concentrations occurred in the early evening. However, variations in plasma ANP values were of relatively small amplitude and not clearly independent of modest parallel shifts in sodium balance. 4. Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. 5. No simple parallel or reciprocal relationships between plasma concentrations of ANP, on the one hand, and concurrent plasma concentrations of other hormones or in the rate of urinary sodium excretion, on the other, were observed during the 25 h of the diurnal study.
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Evans, DH, and Y. Takei. "A Putative Role for Natriuretic Peptides in Fish Osmoregulation." Physiology 7, no. 1 (February 1, 1992): 15–19. http://dx.doi.org/10.1152/physiologyonline.1992.7.1.15.
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Emerging evidence indicates that atrial natriuretic peptide-like peptide hormones may play a significant role in various aspects of fish osmoregulation. Surprisingly, the bulk of current evidence supports a role in salt rather than volume regulation.
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Grimm, Gabriele, Michael Resl, Birgit B. Heinisch, Martin Hülsmann, Anton Luger, Martin Clodi, and Greisa Vila. "B-type natriuretic peptide increases cortisol and catecholamine concentrations in healthy subjects." Journal of Applied Physiology 122, no. 5 (May 1, 2017): 1249–54. http://dx.doi.org/10.1152/japplphysiol.00360.2016.
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B-type natriuretic peptide (BNP) is a hormone released by the heart in response to volume load and exerts natriuretic properties. It is clinically used as a diagnostic and prognostic biomarker and investigated as a pharmacological agent in the therapy of heart failure. Here we investigate the changes in pituitary, adrenal, and thyroid hormones in response to BNP administration in a randomized single-blinded crossover study conducted in ten healthy men aged 21–29 yr. Participants received in two study sessions a continuous intravenous infusion during 4 h (once placebo and once 3 pmol·kg−1·min−1 BNP) and remained in supine position throughout the study. Circulating concentrations of pituitary, adrenal, and thyroid hormones, heart rate, and blood pressure were measured at baseline and hourly afterwards. BNP prevented the physiological decrease in cortisol during the late morning hours leading to elevated serum cortisol levels ( P = 0.022) and increased circulating epinephrine and norepinephrine concentrations ( P = 0.018 and P = 0.036, respectively). These hormone changes were accompanied by an increase in heart rate ( P = 0.019) but no differences in blood pressure. Taken together, the impact of BNP on the endocrine system extends beyond the well-known inhibition of the renin-angiotensin-aldosterone system and includes increased adrenergic activity and cortisol concentrations. This neuroendocrine activation might impact the outcome of therapeutical BNP administrations and should be further investigated in conditions associated with increased BNP secretion. NEW & NOTEWORTHY The heart hormone B-type natriuretic peptide (BNP) is increased in patients with heart failure, where it is thought to have beneficial effects by reducing the preload. Here we report that intravenous administration of BNP in men leads to increases in adrenal hormones cortisol, epinephrine, and norepinephrine. Cortisol and catecholamine levels are independent predictors of increased cardiovascular mortality risk; therefore, drugs targeting the BNP system should be evaluated regarding their effects on the neuroendocrine activation accompanying heart failure.
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Saidova, V. T. "Diagnostic value of natriuretic peptides in pediatrics." Kazan medical journal 94, no. 3 (June 15, 2013): 350–54. http://dx.doi.org/10.17816/kmj2183.
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Natriuretic peptide hormones are the family of vasoactive substanses produced by cardiomyocytes in response to the expansion and increased pressure in the heart chambers. The review of the literature focuses on the diagnostic role of natriuretic peptides in pediatrics. The most important clinical effects of natriuretic peptides, brief history of their discovery and studying, age-related changes of serum levels are analyzed. Data of their use in the diagnosis and cardiac function monitoring in various forms of cardiomyopathy, myocardial inflammatory diseases, Kawasaki disease in children are presented. The results of studies examining the natriuretic peptides levels in children with congenital heart defects and heart transplantation in pre-and postoperative period are reviewed. The review involved the diagnostic use of natriuretic peptides in neonates, including high pulmonary hypertension and hemodynamically significant patent ductus arteriosus diagnosis in preterm infants. The possibility of the natriuretic peptides use for assessing the cardiotoxic complications risk in anti-tumor chemotherapy and for differential diagnosis of acute dyspnea due to heart failure or pulmonary diseases are discussed.
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RADEMAKER, Miriam T., Chris J. CHARLES, Eric A. ESPINER, Chris M. FRAMPTON, M. Gary NICHOLLS, and A. Mark RICHARDS. "Combined inhibition of angiotensin II and endothelin suppresses the brain natriuretic peptide response to developing heart failure." Clinical Science 106, no. 6 (June 1, 2004): 569–76. http://dx.doi.org/10.1042/cs20030366.
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Blockade of AngII (angiotensin II) and ET (endothelin)-1, established and potential therapeutic strategies respectively, for heart failure, may have an adverse effect on the cardiac secretion of the natriuretic peptides, hormones with actions beneficial in this disease. The present study investigates the roles of AngII and ET-1 in regulating the stretch-induced release of the natriuretic peptides during the development of heart failure. On seven separate days, eight sheep underwent incremental left ventricular pacing (155, 190 and 225 beats/min for 90 min each) with concurrent infusions of a vehicle control, AngII, ET-1, AngII+ET-1, losartan [AT1 (AngII type 1) receptor antagonist], bosentan (ETA/ETB receptor antagonist) or losartan+bosentan. Pacing-induced rises in LAP (left atrial pressure) were amplified by the simultaneous administration of separate AngII and ET-1, and attenuated following blockade of the peptides, with maximum effects observed during combined treatments. Although these changes in atrial pressure were paralleled by concomitant alterations in circulating levels of both ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide), the plasma natriuretic peptide/atrial pressure relationship tended to be augmented by AngII and ET-1 and diminished by their blockade. A significant difference was demonstrated between the enhanced plasma BNP response to increasing LAP during combined AngII+ET-1 administration and decreased response during losartan+bosentan treatment (P<0.05). A similar, but non-significant, trend was evident for ANP. The present study indicates dual AngII/ET-1 blockade diminishes BNP (and to a lesser extent ANP) secretion in developing heart failure, suggesting that augmentation of the natriuretic peptide system during the combination of these therapies may be of benefit.
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Takei, Yoshio, and Shigehisa Hirose. "The natriuretic peptide system in eels: a key endocrine system for euryhalinity?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 4 (April 1, 2002): R940—R951. http://dx.doi.org/10.1152/ajpregu.00389.2001.
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The natriuretic peptide system of a euryhaline teleost, the Japanese eel ( Anguilla japonica), consists of three types of hormones [atrial natriuretic peptide (ANP), ventricular natriuretic peptide (VNP), and C-type natriuretic peptide (CNP)] and four types of receptors [natriuretic peptide receptors (NPR)-A, -B, -C, and -D]. Although ANP is recognized as a volume-regulating hormone that extrudes both Na+ and water in mammals, ANP more specifically extrudes Na+ in eels. Accumulating evidence shows that ANP is secreted in response to hypernatremia and acts to inhibit the uptake and to stimulate the excretion of Na+ but not water, thereby promoting seawater (SW) adaptation. In fact, ANP is secreted immediately after transfer of eels to SW and ameliorates sudden increases in plasma Na+ concentration through inhibition of drinking and intestinal absorption of NaCl. ANP also stimulates the secretion of cortisol, a long-acting hormone for SW adaptation, whereas ANP itself disappears quickly from the circulation. Thus ANP is a primary hormone responsible for the initial phase of SW adaptation. By contrast, CNP appears to be a hormone involved in freshwater (FW) adaptation. Recent data show that the gene expression of CNP and its specific receptor, NPR-B, is much enhanced in FW eels. In fact, CNP infusion increases 22Na uptake from the environment in FW eels. These results show that ANP and CNP, despite high sequence identity, have opposite effects on salinity adaptation in eels. This difference apparently originates from the difference in their specific receptors, ANP for NPR-A and CNP for NPR-B. VNP may compensate the effects of ANP and CNP for adaptation to respective media, because it has high affinity to both receptors. On the basis of these data, the authors suggest that the natriuretic peptide system is a key endocrine system that allows this euryhaline fish to adapt to diverse osmotic environments, particularly in the initial phase of adaptation.
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Bold, Adolfo J. de, Mercedes L. Kuroski-de Bold, Poppo H. Boer, Gilles Dubé, Harman Mangat, and Frank Johnson. "A decade of atrial natriuretic factor research." Canadian Journal of Physiology and Pharmacology 69, no. 10 (October 1, 1991): 1480–85. http://dx.doi.org/10.1139/y91-222.
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Present views on the biological significance of atrial natriuretic factor (ANF) relate this polypeptide hormone to the regulation of blood pressure and volume through its modulating effects on renal function, on blood vessel tone and permeability, and on the renin–angiotensin–aldosterone system. Although very important advances in the understanding of ANF have been made over the decade since its discovery, some fundamental facts about ANF biosynthesis and release remain to be elucidated. Stretch-induced enhancement of ANF release appears as the most significant mechanism underlying the endocrine response of the atria to acute volume load. This response decays over a period of minutes, indicating that chronic stimulation of ANF release involves mechanisms different from, or in addition to, those acting during acute stretch-stimulated release. In neither acute nor chronic conditions are the cellular or molecular mechanisms underlying ANF release understood. To better understand long-term stimulation of ANF release, we have conducted extensive in vitro testing of several hormones and neurotransmitters to determine their ability to modify ANF release. From these studies, clear-cut evidence of ANF stimulation was obtained with the vasopressor peptide endothelin. Investigations on the cell and molecular biology of cardiac muscle development and hypertrophy have shown that ANF is involved in cardiac growth. The role played by ANF in these processes is now being determined, but this is one line of evidence that suggests that this hormone, together with other natriuretic peptides, may have autocrine or paracrine functions. Ten years after the discovery of ANF, much remains to be learned not only about ANF biosynthesis but also about details of the interaction of this hormone with its many targets. Nevertheless, the work accomplished to date has produced an astonishingly large amount of new knowledge ranging from new concepts in cell and molecular biology to the development of new therapeutic strategies for the treatment of hypertension and congestive heart failure.Key words: atrial natriuretic peptide, atrial stretch, peptide hormone, tissue culture.
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Choi, Marcelo Roberto, Natalia Lucía Rukavina Mikusic, Nicolás Martín Kouyoumdzian, María Cecilia Kravetz, and Belisario Enrique Fernández. "Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?" BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/710781.
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Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.
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Saito, Yoshihiko, Ichiro Kishimoto, and Kazuwa Nakao. "Roles of guanylyl cyclase-A signaling in the cardiovascular system." Canadian Journal of Physiology and Pharmacology 89, no. 8 (August 2011): 551–56. http://dx.doi.org/10.1139/y11-022.
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Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are cardiac hormones synthesized in and secreted from the heart. ANP and BNP bind the common receptor guanylyl cyclase-A (GC-A) and possess biological actions. Based on their diuretic, natriuretic, and vasodilating activities, they are now widely used as therapeutic agents for heart failure. Roles of endogenous ANP and BNP have been investigated using mice lacking the gene encoding GC-A. Here we describe the recent understanding of roles of GC-A in the cardiovascular system.
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Iacob, Daniela, Angela Butnariu, Daniel-Corneliu Leucuţa, Gabriel Samaşca, Diana Deleanu, and Iulia Lupan. "Evaluation of NT-proBNP in children with heart failure younger than 3 years old." Romanian Journal of Internal Medicine 55, no. 2 (June 1, 2017): 69–74. http://dx.doi.org/10.1515/rjim-2017-0002.
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Abstract Introduction. Heart failure (HF) is characterized by neuroendocrine activation. The cardiac natriuretic hormones, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), together with their related pro-peptides (proANP and proBNP) represent a group of peptide hormones produced by the heart. A normal NT-proBNP level has a high negative predictive value for heart failure. The use of NT-proBNP testing is helpful in diagnosing acute HF in the emergency care setting, allowing an early and optimal treatment. The purpose of this study is to assess the prognostic value of NT-proBNP in heart failure in children younger than 3 years old and to establish whether it correlates with the NYHA/Ross functional class and left ventricle systolic function. Methods. We enrolled 24 consecutive children with HF due to congenital heart diseases and dilated cardiomyopathy. The serum levels of NT-proBNP were measured, all patients underwent echocardiography and left ventricle ejection fraction was calculated. Results. The highest median value of NT-proBNP was recorded in patients with cyanotic heart diseases (248.0 fmol/mL), p = 0.610. NT-proBNP had a negative correlation with the ejection fraction of the left ventricle: Spearman's rank correlation coefficient was −0.165. Conclusions. NT-proBNP levels correlate with the severity of HF in infants and small children younger than 3 years old with heart failure due to congenital heart diseases and dilated cardiomyopathy.
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Schiebinger, R. J., and K. M. Greening. "Interaction between stretch and hormonally stimulated atrial natriuretic peptide secretion." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 1 (January 1, 1992): H78—H83. http://dx.doi.org/10.1152/ajpheart.1992.262.1.h78.
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Atrial stretch and paracrine hormones stimulate atrial natriuretic peptide (ANP) secretion. The potential interplay between atrial stretch and paracrine hormones was examined. Isolated superfused rat left atria paced at 4 Hz were used for study. The effects of 0, 0.5, and 1.5 g settings of initial tension on the ANP secretory response to 1 microM norepinephrine and 10 nM endothelin were examined. The peak ANP secretory responses expressed as a percent of baseline for each of the tension settings were 109 +/- 8, 132 +/- 6, and 171 +/- 10% for norepinephrine and 285 +/- 15, 294 +/- 12, and 368 +/- 19 for endothelin, respectively. The effects of 0.5 microM norepinephrine, 1 nM endothelin, and 100 nM vasopressin on stretch-stimulated secretion were examined. Norepinephrine and endothelin increased ANP secretion 144 +/- 16 and 136 +/- 2% above baseline, respectively. Vasopressin did not increase ANP secretion. Norepinephrine and vasopressin did not significantly influence the ANP secretory response to stretch. In contrast, endothelin increased the response to stretch by 33% (P less than 0.035). We conclude 1) the greater the degree of atrial stretch, the greater is the response to norepinephrine and endothelin; 2) endothelin enhances the secretory response to stretch; and 3) norepinephrine and vasopressin do not affect stretch-stimulated release. These results predict a greater ANP secretory response to hormonal stimulation in vivo in volume-expanded states.
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WONG, Florence, Samuel SIU, Peter LIU, and Laurence M. BLENDIS. "Brain natriuretic peptide: is it a predictor of cardiomyopathy in cirrhosis?" Clinical Science 101, no. 6 (October 29, 2001): 621–28. http://dx.doi.org/10.1042/cs1010621.
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Subtle cardiac abnormalities have been described in patients with cirrhosis. Natriuretic peptide hormones have been reported to be sensitive markers of early cardiac disease. We postulate that plasma levels of N-terminal pro-atrial natriuretic peptide and brain natriuretic peptide could be used as markers of cardiac dysfunction in cirrhosis. The aim of the study was to evaluate the levels of N-terminal pro-atrial natriuretic peptide and brain natriuretic peptide and their relationship with cardiac structure and function in patients with cirrhosis. The study population comprised 36 patients with cirrhosis of mixed aetiologies, but with no cardiac symptoms; 19 of the patients had ascites and 17 did not. The subjects underwent (i) trans-thoracic two-dimensional echocardiography, and (ii) radionuclide angiography for measurements of cardiac structural parameters, diastolic and systolic function. Levels of N-terminal pro-atrial natriuretic peptide and brain natriuretic peptide were also measured. The results were compared with those from eight age- and sex-matched healthy volunteers. Compared with the controls, the baseline mean ejection fraction was increased significantly in both patient groups (P = 0.02), together with prolonged deceleration times (P = 0.03), left atrial enlargement (P = 0.03) and interventricular septal thickening (P = 0.02), findings that are compatible with diastolic dysfunction. Levels of N-terminal pro-atrial natriuretic peptide and brain natriuretic peptide were significantly higher in all patients with cirrhosis with ascites (P = 0.01 and P = 0.05 respectively), but in only some of the pre-ascitic cirrhotic patients, compared with controls. All high levels of brain natriuretic peptide were correlated significantly with septal thickness (P < 0.01), left ventricular diameter at the end of diastole (P = 0.02) and deceleration time (P < 0.01). We conclude that elevated levels of brain natriuretic peptide are related to interventricular septal thickness and the impairment of diastolic function in asymptomatic patients with cirrhosis. Levels of brain natriuretic peptide may prove to be useful as a marker for screening patients with cirrhosis for the presence of cirrhotic cardiomyopathy, and thereby identifying such patients for further investigations.
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Berglund, Hans, Anders Edlund, Elvar Theodorsson, and Hans Vallin. "Haemodynamic and Hormonal Responses to Cardiac Pacing in Humans: Influence of Different Stimulation Sequences and Rates." Clinical Science 88, no. 2 (February 1, 1995): 165–72. http://dx.doi.org/10.1042/cs0880165.
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1. To examine the effects of rate and pressure on release of vasoactive hormones, 10 healthy subjects were examined. 2. A standardized pacing protocol was used to achieve different haemodynamic responses at two predetermined heart rates. Haemodynamic variables, and plasma concentrations of atrial natriuretic peptide, arginine vasopressin, adrenaline and noradrenaline were measured. 3. Right atrioventricular pacing at a rate of 150 impulses/min resulted in disparate responses in right atrial pressure (slight decrease) and pulmonary capillary wedge pressure (increase). Change in arterial plasma concentration of atrial natriuretic peptide correlated to change in pulmonary capillary wedge pressure, and change in arterial plasma concentration of noradrenaline correlated to change in total systemic vascular resistance, whereas concentrations of adrenaline and arginine vasopressin did not alter significantly during the stimulation periods. A significant influence of rate in addition to the pressure related influence on plasma concentration of atrial natriuretic peptide was found. In contrast, an increase in rate in the absence of an increase in atrial pressures did not raise the plasma concentration of atrial natriuretic peptide. There was no significant relationship between change in atrial natriuretic peptide and noradrenaline. 4. These data support the concept of a rate dependence of atrial natriuretic peptide release in man. Increased atrial pressure and thus presumed atrial stretch seems to be a prerequisite for increased plasma concentration of atrial natriuretic peptide. In addition, these results highlight the importance of monitoring both left and right atrial pressure in clinical investigations assessing modulation of atrial natriuretic peptide release.
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Tereschenko, I. V., and N. L. Vladimirskaya. "Hormonal aspects in the pathogenesis of arterial hypertension in young obese patients in young obese patients." Problems of Endocrinology 39, no. 5 (October 15, 1993): 26–28. http://dx.doi.org/10.14341/probl11944.
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Measurements of blood lipids and hormones (plasma renin, aldosterone, vasopressin, prolactin, atrial natriuretic peptide, 6-endorphine, thyrotropin, thyroid hormones) in two groups of patients suffering from obesity (group 1: 64 patients with arterial hypertension and group 2: 26 patients with normal arterial pressure) have brought the authors to a conclusion that arterial hypertension in young obese patients is an early manifestation of essential hypertension. Hormonal dysfunction in obese patients is conducive to early development of essential hypertension in cases when there is a hereditary predisposition to it.
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Ogawa, Tsuneo, Marcelo Vatta, Benoit G. Bruneau, and Adolfo J. de Bold. "Characterization of natriuretic peptide production by adult heart atria." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1977—H1986. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1977.
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The cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are synthesized and costored by atrial cardiocytes and share receptors and many biologic properties. Although some aspects of their synthesis and release are specific for each peptide, it is not clear whether they share intracellular sorting and secretory mechanisms. In the present work we take advantage of a stable isolated rat atrial preparation that allows, for the first time, long-term study of synthesis, trafficking, targeting, and secretion of ANF and BNP by adult atrial muscle. Three model stimuli of secretion were used: increased intra-atrial pressure, endothelin-1 (ET-1), and phenylephrine (PE), representing mechanical, hormonal, and α1-adrenergic stimuli, respectively. To gain further insight into the secretory process under basal and agonist-induced secretion, we employed agents known to inhibit protein synthesis (cycloheximide) or to interfere with the vectorial transport of protein targeted for secretion (brefeldin A and monensin). All these agents induced significant changes in ANF and BNP release. Cycloheximide decreased natriuretic peptide secretion under basal and stimulated conditions. Brefeldin A dramatically increased basal as well as stimulated secretion of ANF and BNP. Monensin partially decreased basal ANF and BNP secretion and completely blocked stimulated secretion. None of these agents modified proteolytic processing as assessed by reverse-phase HPLC analysis. Double-label pulse-chase experiments using [3H]- and [14C]leucine demonstrated that the secretory response to ET-1, in contrast to the response to muscle stretch, is based on peptide other than newly synthesized or relatively newly stored ANF. It is concluded that, in adult atrial cardiocytes, ANF and BNP are sorted to constitutive and regulated pathways in a manner that is substantially unique for atrial cardiocytes. In particular, it appears that basal and stimulated ANF and BNP secretion may have a large “constitutive-like” component, as previously defined in other endocrine systems. This type of secretion is based on the preferential release of hormone through vesicles arising from immature secretory granules. The capacity of the atria to release ANF and BNP in response to stimuli, therefore, may depend more on stimulation of the rate of formation of immature granules than on the amount of stored hormone.
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Tulassay, Tivadar, Wolfgang Rascher, Rudolf E. Lang, Hannsjörg W. Seyberth, and Karl Schärer. "Atrial natriuretic peptide and other vasoactive hormones in nephrotic syndrome." Kidney International 31, no. 6 (June 1987): 1391–95. http://dx.doi.org/10.1038/ki.1987.154.
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Smith, C. P., and R. J. Balment. "Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors." Journal of Endocrinology 136, no. 2 (February 1993): 283–88. http://dx.doi.org/10.1677/joe.0.1360283.
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ABSTRACT The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague–Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1′-methylpropyl)-2-thiobarbiturate) and infused with 0·077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1, d-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [β-mercapto-β,β-cyclopenta-methylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptor subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, All or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis. Journal of Endocrinology (1993) 136, 283–288
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Clerico, Aldo, Fabio A. Recchia, Claudio Passino, and Michele Emdin. "Cardiac endocrine function is an essential component of the homeostatic regulation network: physiological and clinical implications." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 1 (January 2006): H17—H29. http://dx.doi.org/10.1152/ajpheart.00684.2005.
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The discovery of cardiac natriuretic hormones required a profound revision of the concept of heart function. The heart should no longer be considered only as a pump but rather as a multifunctional and interactive organ that is part of a complex network and active component of the integrated systems of the body. In this review, we first consider the cross-talk between endocrine and contractile function of the heart. Then, based on the existing literature, we propose the hypothesis that cardiac endocrine function is an essential component of the integrated systems of the body and thus plays a pivotal role in fluid, electrolyte, and hemodynamic homeostasis. We highlight those studies indicating how alterations in cardiac endocrine function can better explain the pathophysiology of cardiovascular diseases and, in particular of heart failure, in which several target organs develop a resistance to the biological action of cardiac natriuretic peptides. Finally, we emphasize the concept that a complete knowledge of the cardiac endocrine function and of its relation with other neurohormonal regulatory systems of the body is crucial to correctly interpret changes in circulating natriuretic hormones, especially the brain natriuretic peptide.
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Rybkin, Igor I., Mi-Sung Kim, Svetlana Bezprozvannaya, Xiaoxia Qi, James A. Richardson, Craig F. Plato, Joseph A. Hill, Rhonda Bassel-Duby, and Eric N. Olson. "Regulation of atrial natriuretic peptide secretion by a novel Ras-like protein." Journal of Cell Biology 179, no. 3 (November 5, 2007): 527–37. http://dx.doi.org/10.1083/jcb.200707101.
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Atrial cardiomyocytes, neurons, and endocrine tissues secrete neurotransmitters and peptide hormones via large dense-core vesicles (LDCVs). We describe a new member of the Ras family of G-proteins, named RRP17, which is expressed specifically in cardiomyocytes, neurons, and the pancreas. RRP17 interacts with Ca2+-activated protein for secretion-1 (CAPS1), one of only a few proteins known to be associated exclusively with LDCV exocytosis. Ectopic expression of RRP17 in cardiomyocytes enhances secretion of atrial natriuretic peptide (ANP), a regulator of blood pressure and natriuresis. Conversely, genetic deletion of RRP17 in mice results in dysmorphic LDCVs, impaired ANP secretion, and hypertension. These findings identify RRP17 as a component of the cellular machinery involved in regulated secretion within the heart and potential mediator of the endocrine influence of the heart on other tissues.
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Stokes, G. S., J. C. Monaghan, and D. N. Pillai. "Comparison of the Effects on Urinary Sodium Excretion of Indomethacin and of Carbidopa in normal Volunteers given an Intravenous Saline Infusion." Clinical Science 92, no. 4 (April 1, 1997): 409–14. http://dx.doi.org/10.1042/cs0920409.
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1. Dopamine and prostaglandins are putative endogenous natriuretic hormones. The role of each in facilitating natriuresis induced by intravenous saline infusion was examined in normal volunteers in relation to administration of carbidopa, a dopadecarboxylase inhibitor, and indomethacin, an inhibitor of prostaglandin synthetase. 2. In a placebo-controlled, randomized study, 13 subjects received carbidopa (100 mg) and 12 received indomethacin (50 mg). Proximal and distal renal tubular Na+ reabsorption were determined using exogenous lithium clearance. 3. On the control day, 2 litres of 0.9% saline (308 mmol Na+) given intravenously in 3 h, resulted in volume expansion and natriuresis. Carbidopa reduced the urinary dopamine/noradrenaline ratio but showed no anti-natriuretic effect and no effect on fractional Na+ reabsorption. Indomethacin diminished natriuresis and increased distal fractional Na+ reabsorption in proportion to the anti-natriuretic effect. 4. The changes in plasma concentrations of albumin, aldosterone, atrial natriuretic peptide and renin activity associated with volume expansion were not modified by either carbidopa or indomethacin. Urinary prostaglandin E2 excretion was decreased transiently by indomethacin and was unaffected by carbidopa. 5. This study suggests that prostaglandins may modulate urinary Na+ excretion during saline-induced natriuresis through inhibition of distal tubular Na+ reabsorption. No role for free dopamine as a modulator of renal Na+ handling could be assigned on the basis of the findings with carbidopa.
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Sindic, Aleksandra. "Current Understanding of Guanylin Peptides Actions." ISRN Nephrology 2013 (April 17, 2013): 1–17. http://dx.doi.org/10.5402/2013/813648.
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Guanylin peptides (GPs) family includes guanylin (GN), uroguanylin (UGN), lymphoguanylin, and recently discovered renoguanylin. This growing family is proposed to be intestinal natriuretic peptides. After ingestion of a salty meal, GN and UGN are secreted into the intestinal lumen, where they inhibit sodium absorption and induce anion and water secretion. At the same conditions, those hormones stimulate renal electrolyte excretion by inducing natriuresis, kaliuresis, and diuresis and therefore prevent hypernatremia and hypervolemia after salty meals. In the intestine, a well-known receptor for GPs is guanylate cyclase C (GC-C) whose activation increases intracellular concentration of cGMP. However, in the kidney of GC-C-deficient mice, effects of GPs are unaltered, which could be by new cGMP-independent signaling pathway (G-protein-coupled receptor). This is not unusual as atrial natriuretic peptide also activates two different types of receptors: guanylate cylcase A and clearance receptor which is also G-protein coupled receptor. Physiological role of GPs in other organs (liver, pancreas, lung, sweat glands, and male reproductive system) needs to be discovered. However, it is known that they are involved in pathological conditions like cystic fibrosis, asthma, intestinal tumors, kidney and heart failure, obesity, and metabolic syndrome.
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Coyle, S., M. D. Penney, P. W. Masters, and B. E. Walker. "Early diagnosis of ectopic arginine vasopressin secretion." Clinical Chemistry 39, no. 1 (January 1, 1993): 152–54. http://dx.doi.org/10.1093/clinchem/39.1.152.
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Abstract We describe a patient who presented with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) 2 months before clinical evidence of bronchogenic malignancy. Because of the potential for the ectopic production of atrial natriuretic peptide (ANP) to mimic SIADH, both hormones were measured in this hyponatremic patient to seek a possible marker of tumor activity. A hypertonic saline infusion at presentation revealed excessive osmotically decoupled secretion of arginine vasopressin but a normal ANP response.
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Polak, J., C. Moro, E. Klimcakova, M. Kovacikova, M. Bajzova, M. Vitkova, Z. Kovacova, et al. "The atrial natriuretic peptide- and catecholamine-induced lipolysis and expression of related genes in adipose tissue in hypothyroid and hyperthyroid patients." American Journal of Physiology-Endocrinology and Metabolism 293, no. 1 (July 2007): E246—E251. http://dx.doi.org/10.1152/ajpendo.00688.2006.
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Thyroid dysfunction is associated with several abnormalities in intermediary metabolism, including impairment of lipolytic response to catecholamines in subcutaneous abdominal adipose tissue (SCAAT). Atrial natriuretic peptide (ANP) is a powerful lipolytic peptide; however, the role of ANP-mediated lipolysis in thyroid disease has not been elucidated. The aim of this study was to investigate the role of thyroid hormones in the regulation of ANP-induced lipolysis as well as in the gene expression of hormone-sensitive lipase, phosphodiesterase 3B (PDE3B), uncoupling protein-2 (UCP2), natriuretic peptide receptor type A, and β2-adrenergic receptor in SCAAT of hyperthyroid and hypothyroid patients. Gene expression in SCAAT was studied in 13 hypothyroid and 11 hyperthyroid age-matched women before and 2–4 mo after the normalization of their thyroid status. A microdialysis study was performed on a subset of nine hyperthyroid and 10 hypothyroid subjects. ANP- and isoprenaline-induced lipolyses were higher in hyperthyroid subjects, with no differences between the groups following treatment. Hormone-sensitive lipase gene expression was higher in hyperthyroid compared with hypothyroid subjects before treatment, whereas no difference was observed following treatment. No differences in gene expression of other genes were observed between the two groups. Following treatment, the gene expression of UCP2 decreased in hyperthyroid, whereas the expression of PDE3B decreased in hypothyroid subjects. We conclude that thyroid hormones regulate ANP- and isoprenaline-mediated lipolysis in human SCAAT in vivo. Increased lipolytic subcutaneous adipose tissue response in hyperthyroid patients may involve postreceptor signaling mechanisms.