Relevant bibliographies by topics / Natriuretic peptide hormones

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Academic literature on the topic 'Natriuretic peptide hormones'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Natriuretic peptide hormones"

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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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2

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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Dissertations / Theses on the topic "Natriuretic peptide hormones"

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Hove, Runyararo Memory. "Evolutionary development and functional role of plant natriuretic peptide (PNP)-B." Thesis, University of Fort Hare, 2009. http://hdl.handle.net/10353/155.

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Plant natriuretic peptides (PNP) are novel peptides which, like in vertebrates, have been shown to have a function associated with water and salt homeostasis. Two PNP-encoding genes have been identified and isolated from Arabidopsis thaliana, namely; AtPNP-A and AtPNP-B. In this study, the focus was on PNP-B, which has not been extensively studied. Bioinformatic analysis was done on the AtPNP-B gene. This included the bioinformatic study of its primary structure, secondary structure, tertiary structure, transcription factor binding sites (TFBS) and its relation to other known proteins. The AtPNP-B gene was shown to be a 510 bp long, including a predicted 138 bp intron. AtPNP-B was also shown to have some sequence similarity with AtPNP-A and CjBAp12. The TFBS for AtPNP-B and OsJPNP-B were compared and they comprised of TFBS that are related to water homeostasis and pathogenesis. This suggested two possible functions; water stress and homeostasis and a pathogenesis related function for PNP-B. Following bioinformatic analysis, the heterologous expression of the AtPNP-B was attempted to investigate whether the AtPNP-B gene encoded a functional protein and to determine the functional role of PNP-B. However, expression was unsuccessful. An evolutionary study was then carried out which revealed that there were some plants without the intron such as, rice, leafy spurge, oilseed rape, onion, poplar, sugar cane, sunflower and tobacco. These plants would therefore be used for expression and functional studies in the future. The evolutionary studies also revealed that PNP-B had a relationship with expansins and the endoglucanase family 45. Other PNP-B related molecules were also obtained from other plant genomes and therefore used in the construction of a phylogenetic tree. The phylogenetic tree revealed that AtPNP-B clustered in the same group as CjBAp12 while AtPNP-A had its own cluster group. There were also other PNP-B like molecules that clustered in the same group as expansins (α- and β-). Thus, we postulate that, like PNP-A, PNP-B also has a possible function in water and salt homeostasis. However, due to the clustering iii of AtPNP-B into the same group as CjBAp12, a possible role of PNP-B in pathogenesis-related response is also postulated.
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Pharmawati, Made, and mikewood@deakin edu au. "A study of the natriuretic peptide hormone system in plants." Deakin University. School of Biological and Chemical Sciences, 1999. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20060727.145040.

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In this study, both physiological and cellular effects are elicited by natriuretic peptides (NPs), a novel type of plant hormone. It was found that rat ANP (rANP) influenced stomatal opening movement in Tradescantia sp., where a significant increase in stomatal opening was observed in the presence of 1 µM rANP. Furthermore, this effect is mediated by cGMP, a (putative) second messenger of NPs. Two inhibitors of guanylyl cyclase, LY 83583 and methylene blue, inhibited rANP-induced stomatal opening. In contrast, stomatal opening is induced in a concentration dependent manner by the cell permeant cGMP analogue 8-Br-cGMP. In addition it was found, that like in animals, the secondary structure of rANP is essential for rANP responses. Linearised rANP is biologically inactive. Since ANP elicit plant responses, an attempt was made to isolate NP analogues from plants. A protocol for partially purifying NP from plants was developed. It was found that two fractions eluted from an immunoaffinity chromatography column (0.5 M KCI eluted fraction and 0.75 M KCI eluted fraction) were biologically active. The level of cGMP in response to NPs was also tested. It is suggested that the receptor of NP is specific since only 0.75 M KCI eluted fractions increased cGMP levels in Zea mays root stele tissue. rANP did not elicit an effect on cGMP levels in this tissue and LY 83583 did not affect this response. It is therefore argued that a plant specific biologically active NP system is present in the stele and it is predicted that NPs modulate solute movement in this tissue. NPs also influence K+, Na+ and H+ fluxes in Zea mays root stele. Increase in both K+ and Na+ uptake were observed after 30 min., while H+ flux shifted immediately toward influx in the presence of both 0.5 and 0.75 KCI eluted fractions. Finally, a model is proposed for the effect of NPs on solute movement and its signalling system in plants.
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Bastian, René. "Characterisation of AtPNP-A - a novel arabidopsis thaliana gene with role in water and salt homeostasis." Thesis, University of the Western Cape, 2009. http://hdl.handle.net/11394/2818.

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Philosophiae Doctor - PhD
Plant natriuretic peptides (PNPs) are a novel class of extracellular, systemically mobile molecules that elicit a number of plant responses important in homeostasis and growth. Natriuretic peptides were first identified in vertebrates where they play a role in the regulation of salt and water balance. Subsequent experimental investigations have identified the presence of a natriuretic peptide hormone system in plants. While PNPs have been implicated in various physiological responses such as stomatal guard cell movements and regulation of net water uptake, its biological role has remained elusive. Here we have used co-expression and promoter content analysis tools to understand the biological role of the Arabidopsis thaliana PNP (AtPNP-A). The analysis of AtPNP-A and its co-expressed genes revealed that genes annotated as part of the systemic acquired resistance (SAR) pathway were over-represented, thus suggesting that AtPNP-A may function as a component of plant defense responses and specifically, SAR. The results further show that AtPNP-A shares many characteristics with pathogenesis related (PR) proteins in that its transcription is strongly induced in response to pathogen challenges, thus implying a newly described role for AtPNP-A in pathogen attack. Additional tissue expression analysis also indicated distinct localization of PNP activity in sepals and transcriptional meta-analysis showed that AtPNP-A may play a role in starch breakdown. Therefore, together with the finding that AtPNP-A plays a role in regulating phloem transport, we also hypothesize that AtPNP-A may play a role in phloem unloading in sepals to assist processes such as seed formation in plants. In plants, the second messenger, guanosine 3’,5’-cyclic monophosphate (cGMP) mediates a whole range of important processes including salinity tolerance, disease resistance, drought tolerance and responses to light. Since PNPs regulate water and salt homeostasis via a cGMP-dependent signaling pathways, it is thus important to analyse the transcriptome induced by the second messenger (cGMP) in Arabidopsis thaliana to give a better understanding of its mechanism of action. This study was also supplemented by the analysis of the gibberellic acid (GA) dependent transcriptome, since cGMP also plays a role its transcription pathway. This data analysis, together with promoter content investigation, revealed that genes upregulated after cGMP treatment and down-regulated in the GA insensitive mutant (ga1-3) were enriched with a GA response element (GARE), while no GARE enrichment were observed in genes up-regulated in the ga1-3 mutant. These findings suggest that GARE is indicative of GA-induced and cGMP-dependent transcriptional up-regulation. Gene ontology analysis confirmed previous reports that cGMP is involved in ion homeostasis and indicated that the transcriptional cGMP response is bi-polar in the sense that both genes up- and down-regulated in response to cGMP is involved in cation transport. Additionally, ab initio analysis of genes transcriptionally dependent on cGMP identified CHX8 as a hub gene and promoter content of CHX8 co-expressed genes show enrichment of the GARE motif. The fact that CHX8 has its highest expression levels during male gametogenesis and pollen tube growth, together with our findings, suggest that GA-induced and cGMP- dependent genes may play a key role in ion and water homeostasis in the male gametophyte. Finally, we propose that the type of analysis undertaken here can yield new insights into gene regulation networks and inform experimental strategies to unravel complex transcription regulatory systems under different developmental and stimulus specific conditions.
South Africa
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Mellor, Adrian John. "Hormonal adaptation to acute and chronic hypoxia : the role of brain natriuretic peptide and stress hormones in the diagnosis and etiology of altitude illness." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3202.

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Data was collected in two main phases; 1. A field study undertaken in the Cordillera Real Region of Bolivia. 2. Laboratory investigation of terrestrial, hypobaric and normobaric hypoxia. Phase 1 The aim of phase one of the studies was to investigate the endocrine changes (specifically brain natriuretic peptide (BNP), arginine vasopressin (AVP), cortisol, catecholamine and copeptin) with ascent to high altitude. These changes were investigated during a “real world” trekking expedition to Bolivia. Other potential markers for AMS namely high-sensitivity C reactive protein (hs-CRP), high-sensitivity cardiac troponin T (hs-cTnT) and neutrophil gelatinase associated lipocalin (NGAL) were also studied. The overarching hypothesis was that Acute Mountain Sickness (AMS) would be associated with fluid retention and elevated BNP and that changes in other hormones involved in fluid balance such as AVP, copeptin and cortisol may also reflect AMS. The hypotheses investigated included;  That BNP would rise with high altitude (HA) illness and be associated with both AMS and a high pulmonary artery systolic pressure (PASP).  That copeptin would accurately reflect changes in AVP at altitude and therefore have utility in future field studies as a surrogate for AVP.  That AMS would be associated with either elevated copeptin/AVP or with failure to suppress the copeptin/AVP response to exercise.  Inflammation and/or rises in PASP occur with the development of high altitude illness and would lead to a detectable rise in hs-cTnT, NGAL or hs-CRP.  The dynamic changes in stress hormones associated with exercise are key in the pathogenesis of altitude illness.  The physiological stress of HA would lead to a rise in cortisol. This would contribute to fluid retention and be linked to the development of AMS.  There would be no difference between total body water (TBW) measured by single or multifrequency bioimpedance analysis. v Methods: This was an observational study with data collection at sea-level and then subsequently over a 10 day ascent from 3800m to 5129m. Daily physiological data was collected with more detailed investigation performed at 3833m, 4450m and 5129m. At these altitudes, data was collected post exercise (after the ascent) and at rest (the following day). Venous blood samples were collected for hormonal assays. BNP and NGAL were analysed in situ using point of care testing technology. Assessment of TBW was performed using bioimpedance devices and pulmonary artery systolic pressure (PASP) was estimated using transthoracic echocardiography. Results and implications: 50 subjects were recruited to the study, 48 of whom were studied at 3833m and 4450m with 47 subjects studied at 5129m. Results presented as mean (range, SD) unless otherwise stated. Significant findings were: Oxygen saturations fell with ascent to altitude to a nadir of 79% (SD 4.4., range 68-88) at 5129m. Fluid balance showed no significant change with altitude or relation to AMS. Plasma osmolality did not change with ascent. AVP and copeptin did not increase until extreme altitude (5129m) and both increased by a greater degree in those recording higher levels of perceived exertion. This was despite no change in osmolality which suggests a non-osmotic stimulus to their secretion. Cortisol secretion increased at 5129m and may support the possibility that the rise in copeptin and AVP was related to physiological stress at extreme altitude. Plasma normetanephrine increased with increasing altitude reaching a maximum of 1423.72 (786.0, 355–4159 pmol/L) at 5129m. Thirst proved difficult to quantify and the visual analogue scale used showed no correlation with total body water, osmolality or AVP. BNP (and NT-proBNP) increased with increasing severity of AMS as assessed by Lake Louise Score (LLS). vi BNP (and NT-proBNP) were higher in those with a high PASP. Hs-cTnT showed an increase with PASP and but no association with AMS. Hs-CRP showed an increase with altitude but no association with AMS. NGAL showed no association with change in altitude. A consistent finding was an evident separation between subjects recording a low Borg score and those recording a Borg rating consistent with “hard work”. Subjects recording a Borg score > 15 (“hard work”) had higher cortisol, AVP, copeptin and an increased LLS. This led to investigation of an additional hypothesis that a higher rating of perceived exertion will lead to an increase in reported AMS symptoms. This was found to be the case with significantly lower SpO2 at rest, higher heart rates and higher LLS in those reporting a Borg RPE > 15.
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Netchitailo, Pierre. "La corticostéroïdogénèse chez un amphibien anoure : mécanismes intracellulaires et contrôle multifactoriel." Rouen, 1987. http://www.theses.fr/1987ROUES037.

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Fan, Xiaohui. "Uroguanylin : molecular cloning and characterization of a potential natriuretic hormone /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841285.

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7

Ruzvidzo, Oziniel. "Plant Natriuretic Peptides - Elucidation of the Mechanisms of Action." Thesis, University of the Western Cape, 2009. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5854_1285860491.

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Several lines of cellular and physiological evidence have suggested the presence of a novel class of systemically mobile plant molecules that are recognized by antibodies generated against vertebrate atrial natriuretic peptides (ANPs). Functional characterization of these immunoanalogues, referred to as immunoreactive plant natriuretic peptides (irPNPs) or plant natriuretic peptides (PNPs), has shown that they play important roles in a number of cellular processes crucial for plant growth and maintenance of cellular homeostasis. Although the various biological roles of PNPs in plants are known, their exact mode of action remains elusive. To elucidate the mechanisms of action for these immunoanalogues, we have prepared a biologically active recombinant PNP from Arabidopsis thaliana (AtPNP-A) and the biological activity was demonstrated by showing its ability to induce water uptake into Arabidopsis thaliana protoplasts. In addition, the molecule was shown to downregulate photosynthesis while at the same time up-regulating respiration, transpiration as well as net water uptake and retention capacities in the sage Plectranthus ecklonii. Further analysis of the recombinant AtPNP-A indicated that the peptide can induce systemic response signalling though the phloem. A recombinant Arabidopsis wall associated kinase-like protein (AtWAKL10) that has a domain organization resembling that of vertebrate natriuretic peptide (NP) receptors was also partially characterized as a possible receptor for the recombinant AtPNP-A. Vertebrate NP receptors contain an extracellular ligand-binding domain and an intracellular guanylate cyclase (GC)/kinase domain and signal through the activity of their GC domain that is capable of generating intracellular cGMP from GTP. The structural resemblance of AtWAKL10 to vertebrate NP receptors could suggest a functional homology with receptor molecules and it is conceivable that such a receptor may recognize PNPs as ligands. The characterization of the recombinant AtWAKL10 showed that the molecule functions as both a GC and a kinase in vitro. This strengthened the suggestion that AtWAKL10 could be a possible AtPNP-A receptor especially considering the fact that AtPNP-A applications to plant cells also
trigger cGMP transients. Furthermore, a bioinformatic analysis of the functions of AtPNP-A and AtWAKL10 has inferred both molecules in plant pathogen responses and defense mechanisms, thus indirectly functionally linking the two proteins.

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Zhang, Jin. "Inhibition of pulsatile luteinizing hormone release by atrial natriuretic peptide and brain natriuretic peptide in the ovariectomized rat." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29412.

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Atrial natriuretic peptide (ANP) of atrial myocyte origin, has been shown to play a role in the diuresis, natriuresis, and antagonism of angiotensin and vasopressin. However, it is now apparent that in addition to the production of the peptide in the heart and in its role in fluid and electrolyte homeostasis, it is also produced in the central nervous system participating in the regulation of pituitary hormone secretion. Administration of ANP through both central and peripheral routes has been shown to inhibit secretion of luteinizing hormone (LH) in the gonadectomized rat model. A better understanding of the modulatory role of ANP on LH secretion and its possible mechanisms will add to our knowledge of the effects of neuropeptides on reproductive function. Brain natriuretic peptide (BNP) is a bioactive peptide of 26 amino acid residues recently identified in porcine brain. The peptide exerts potent diuretic-natriuretic and vasorelaxant effects, in a manner similar to that of ANP. BNP has a remarkable high sequence homology to ANP, especially in the 17 amino acid ring formed by an intramolecular disulfide linkage which is required for biological activity. The presence of BNP with ANP in the mammalian brain and remarkable resemblance in their molecular structures and physiological functions implies that BNP may also exert an inhibitory effect on LH secretion like ANP. This research focused on the effects of centrally administered ANP and BNP on pulsatile LH secretion and their possible mechanisms of action in ovariectomized rats. After third ventricle infusion of ANP or BNP, inhibition of mean plasma LH level, LH pulse amplitude and pulse frequency was observed. In searching for the possible mechanisms of inhibitory effect of ANP or BNP on pulsatile LH secretion, the effect of inhibiting the endogenous opiate system with naloxone on the action of centrally administered ANP or BNP was tested. Application of naloxone reversed the inhibitory effect of ANP and BNP on mean plasma LH level and LH pulse amplitude, but in terms of pulse frequency, naloxone treatment failed to reverse the inhibitory effect of ANP or BNP. In separate experiments, pretreatment with pimozide, a dopaminergic receptor blocker, prevented the inhibitory action of ANP and BNP on LH secretion. After infusion of ANP or BNP, there were no significant decrease in mean plasma LH level, pulse amplitude and pulse frequency in the pimozide-pretreated rats. In summary, the present study shows that both ANP and BNP inhibit pulsatile LH secretion, suggesting that the inhibitory effects on LH secretion once thought to be mediated by ANP alone may be regulated through a dual mechanism involving both ANP and BNP. Furthermore, the inhibitory mechanisms may involve the interactions of ANP and BNP with central opiate system and dopaminergic system on LH secretion.
Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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9

Taskinen, P. (Panu). "Mapping the cellular mechanisms regulating atrial natriuretic peptide secretion." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:9514252721.

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Abstract Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are cardiac hormones, which are involved in the regulation of blood pressure and fluid homeostasis. The major determinant for ANP and BNP release are atrial and ventricular wall stretch, but also some vasoactive factors such as endothelin-1 (ET-1) can enhance cardiac hormone secretion. The mechanical stretch rapidly activates multiple signal transduction pathways in cardiac cells, but the cellular mechanisms mediating stretch-induced ANP secretion are still unknown. The aim of the present study was to examine the cellular mechanisms of autocrine/paracrine factors and stretch-induced ANP secretion. Genistein, a potent protein tyrosine kinase (PTK) inhibitor, rapidly increased cardiac contractile force and ANP secretion in perfused rat heart. This effect of genistein may be unrelated to the inhibition of PTKs since this stimulation was blocked by a L-type calcium channel antagonist and Ca2+/calmodulin-dependent protein kinase II inhibitor. Pregnancy hormone relaxin increased heart rate and ANP secretion in perfused spontaneously beating heart, suggesting that relaxin may have a role in modulating cardiac function. Cellular mechanisms of atrial wall stretch-induced ANP secretion were also studied. This enhanced secretion was blocked by sarcoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin and PTK inhibitor lavendustin A, indicating that thapsigargin sensitive Ca2+ pools and activation of PTK orPTK cascade have an important role in the regulation of stretch-secretion coupling. In addition, protein phosphatase inhibitor okadaic acid accelerated stretch-induced ANP secretion, suggesting that precise balance of protein kinase and phosphatase activity plays a role in mechanical stretch-induced ANP secretion. Finally interactions of endothelial factors regulating ANP exocytosis were studied. The potent nitric oxide synthase inhibitor L-NAME increased basal and atrial wall stretch-induced ANP secretion in the presence of ET-1, suggesting that nitric oxide may tonically inhibit ANP secretion.
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Zhang, Yi. "Implications of natriuretic peptides and endothelin-1 release during myocardial ischaemia." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phz6334.pdf.

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Addenda and corrigenda are tipped-in & numbered leaves 281-282. Copies of author's previously published articles are inserted back end paper. Bibliography: leaves 222-279. Studies were performed in the Langendorff-perfused isolated rat heart, using a paradigm in which atrial distension was prevented. The release of natriuretic peptides and endothelin-1, along with cardiac function was monitored during periods of transient ischaemia or hypoxia. Additional studies were performed in patients undergoing cardiac catheterization.
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Books on the topic "Natriuretic peptide hormones"

1

Atrial natriuretic hormones. Englewood Cliffs, NJ: Prentice Hall, 1992.

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F, Mantero, and Vecsei Pál, eds. Corticosteroids and peptide hormones in hypertension. New York: Raven Press, 1987.

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Rahimi, Kazem. Chronic heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0092.

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The European Society of Cardiology defines heart failure as a clinical syndrome in which patients have the following features: symptoms typical of heart failure (breathlessness, fatigue, ankle swelling); signs typical of heart failure (tachycardia, tachypnoea, pulmonary crackles, pleural effusion, raised jugular venous pressure, peripheral oedema, hepatomegaly); and objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heat sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration). Heart failure results in activation of the sympathetic nervous system and the renin–aldosterone–angiotensin system, and release of a number of hormones such as natriuretic peptides, and cytokines, including tumour necrosis factor amongst others. While neurohormone activation is initially compensatory and helps in the short term to maintain circulatory needs, ultimately it has detrimental effects on the myocardium and compromises its function further. These mechanisms are therefore therapeutic targets to improve symptoms and lessen the risk of death.
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Nishikimi, Toshio. Adrenomedullin in Cardiovascular Disease (Basic Science for the Cardiologist). Springer, 2005.

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J, Mulrow Patrick, and Schrier Robert W, eds. Atrial hormones and other natriureticfactors. Bethesda, Md: American Physiological Society, 1987.

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1926-, Mulrow Patrick J., and Schrier Robert W, eds. Atrial hormones and other natriuretic factors. Bethesda, Md: American Physiological Society, 1987.

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Clerico, Aldo, and Michele Emdin. Natriuretic Peptides: The Hormones of the Heart. Springer, 2006.

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Clerico, Aldo, and Michele Emdin. Natriuretic Peptides: The Hormones of the Heart. Springer, 2010.

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Hormones and the Heart in Health and Disease (Contemporary Endocrinology). Humana Press, 1999.

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Diseases of the Pituitary: Diagnosis and Treatment. Humana Press, 2011.

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Book chapters on the topic "Natriuretic peptide hormones"

1

Lang, R. E., H. Ruskoaho, M. Toth, D. Ganten, T. Unger, and R. Dietz. "Mechanisms Controlling Release of Atrial Natriuretic Peptide." In Atrial Hormones and Other Natriuretic Factors, 19–31. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_3.

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Kam, Peter, Ian Power, Michael J. Cousins, and Philip J. Siddal. "Erythropoietin, Atrial Natriuretic Peptide and Sex Hormones." In Principles of Physiology for the Anaesthetist, 395–96. Fourth edition. | Boca Raton : CRC Press, Taylor & Francis Group, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429288210-64.

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Espiner, Eric A., M. Gary Nicholls, A. Mark Richards, Ross C. Cuneo, Tim G. Yandle, and Hamid Ikram. "Effect of Human Atrial Natriuretic Peptide in Normal and Hypertensive Humans." In Atrial Hormones and Other Natriuretic Factors, 117–25. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_11.

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Kramer, H. J., H. Meyer-Lehnert, and H. G. Predel. "Natriuretic Hormones: Endogenous Na-K-ATPase Inhibitor(s) and Atrial Natriuretic Peptide." In Endocrinology of the Heart, 78–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83858-3_9.

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Evans, D. H. "The Roles of Natriuretic Peptide Hormones in Fish Osmoregulation and Hemodynamics." In Mechanisms of Systemic Regulation: Acid—Base Regulation, Ion-Transfer and Metabolism, 119–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-52363-2_6.

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Seino, M., K. Abe, N. Nushiro, K. Omata, S. Itoh, and K. Yoshinaga. "Interaction of Calcium Ion and Atrial Natriuretic Peptide on Blood Pressure, Natriuresis and the Renal Kallikrein-Kinin System in Anesthetized Rabbits." In Vasodepressor Hormones in Hypertension: Prostaglandins and Kallikrein-Kinins, 239–46. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9299-5_25.

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Saavedra, J. M. "Interactions Between the Circulating Hormones Angiotensin and Atrial Natriuretic Peptide and Their Receptors in Brain." In Advances in Experimental Medicine and Biology, 191–210. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5799-5_12.

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Ballermann, Barbara J., B. Rentz Dunn, Ramon E. Mendez, Mark L. Zeidel, Julian L. Seifter, and Barry M. Brenner. "Renal Actions of Atrial Natriuretic Peptides." In Atrial Hormones and Other Natriuretic Factors, 83–92. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_8.

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Thibault, Gaétan, Raul Garcia, Ernesto L. Schiffrin, Andre De Léan, Peter W. Schiller, Jolanta Gutkowska, Jacques Genest, and Marc Cantin. "Structure-Activity Relationships of Atrial Natriuretic Peptides." In Atrial Hormones and Other Natriuretic Factors, 77–82. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_7.

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Mulrow, Patrick J., Roberto Franco-Saenz, K. Atarashi, Masao Takagi, and Mari Takagi. "Effect of Atrial Peptides on the Adrenal Cortex." In Atrial Hormones and Other Natriuretic Factors, 93–109. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_9.

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