Academic literature on the topic 'Atrial natriuretic peptides; Respiratory organs – Physiology'
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Journal articles on the topic "Atrial natriuretic peptides; Respiratory organs – Physiology"
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Mendelsohn, F. A. O., A. M. Allen, S. Y. Chai, P. M. Sexton, and R. Figdor. "Overlapping distributions of receptors for atrial natriuretic peptide and angiotensin II visualized by in vitro autoradiography: morphological basis of physiological antagonism." Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1517–21. http://dx.doi.org/10.1139/y87-239.
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Atrial natriuretic peptides exert actions on many key organs involved in blood pressure and water and electrolyte balance. Many of these actions result in a physiological antagonism of angiotensin. To investigate the morphological basis of this interaction, we have mapped the distribution of receptors for atrial natriuretic peptide and angiotensin II in a number of target organs, using 125I-labelled rat atrial natriuretic peptide (99–126) and 125I-labelled [Sar1,Ile8]angiotensin II. In the kidney both atrial natriuretic peptide and angiotensin II receptors were observed overlying glomeruli, vasa recta bundles (high densities), and the outer cortex (moderate density). In the other tissues studied, atrial natriuretic peptide and angiotensin II receptors were codistributed in the adrenal zona glomerulosa, cerebral circumventricular organs including the subfornical organ, organum vasculosum of the lamina terminalis and area postrema, and the external plexiform layer of the olfactory bulb. The concurrent distribution of specific receptors for both peptides at these sites provides the basis for atrial natriuretic peptide to exert a functional antagonism of the actions of angiotensin II on blood pressure and water and electrolyte homeostasis at multiple sites.
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Goetz, K. L. "Physiology and pathophysiology of atrial peptides." American Journal of Physiology-Endocrinology and Metabolism 254, no. 1 (January 1, 1988): E1—E15. http://dx.doi.org/10.1152/ajpendo.1988.254.1.e1.
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The atria secrete atrial peptides (atriopeptins) that are capable of producing dramatic alterations in a number of body processes. Secretion of atriopeptin appears to be regulated primarily by the prevailing pressure within the atria. In pharmacological doses, atriopeptin rapidly elicits a natriuresis when administered to experimental animals or humans. In contrast, infusion rates that increase plasma atriopeptin only by about three- to fivefold tend to produce a slowly developing and modest diuresis. Evidence examined in this review suggests that the atrial peptides are not potent natriuretic substances under normal physiological conditions, although it is likely that they exert a modulating influence on sodium excretion. The atrial peptides are vasoactive and induce a number of cardiovascular changes including decreases in arterial blood pressure, cardiac filling pressure, and cardiac output and a translocation of fluid from plasma to the interstitial fluid space. They also interact with other hormones, particularly the renin-angiotensin-aldosterone system. Finally, atriopeptin is distributed throughout many regions of the brain where it may serve as a neuromodulator or neurotransmitter. Atriopeptin circulating in the bloodstream also may influence cerebral mechanisms by acting on receptors in the circumventricular organs. A more complete understanding of the diverse effects of this cardiac endocrine system is expected to provide further insight into a spectrum of physiological and pathophysiological processes.
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Chabrier, P. E., P. Roubert, P. Plas, and P. Braquet. "Blood–brain barrier and atrial natriuretic factor." Canadian Journal of Physiology and Pharmacology 66, no. 3 (March 1, 1988): 276–79. http://dx.doi.org/10.1139/y88-047.
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In brain, binding sites for atrial natriuretic factor (ANF) have been characterized in areas such as circumventricular organs that lack the tight capillary endothelial junctions of the blood–brain barrier and therefore are exposed to circulating peptides. Since atrial natriuretic factor acts directly on vascular endothelium and has been proposed to be actively involved in blood pressure regulation and fluid homeostasis, it is interesting to know whether ANF receptors exist on brain capillaries that constitute the blood–brain barrier and participate in the constant fluid exchange between blood and brain. The present paper reports recent evidence of the presence of ANF receptors located on the structure. It assesses the specific binding of 125I-labelled ANF on bovine brain microvessel preparations and its coupling with a guanylate cyclase system. The potential physiological role of ANF on brain microcirculation and blood–brain barrier functions is discussed.
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Filippatos, Gerasimos S., Nupur Gangopadhyay, Omosalewa Lalude, Narayanan Parameswaran, Sami I. Said, William Spielman, and Bruce D. Uhal. "Regulation of apoptosis by vasoactive peptides." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 4 (October 1, 2001): L749—L761. http://dx.doi.org/10.1152/ajplung.2001.281.4.l749.
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Although originally discovered because of their ability to affect hemodynamics, vasoactive peptides have been found to function in a variety of capacities including neurotransmission, endocrine functions, and the regulation of cell proliferation. A growing body of evidence describes the ability of vasoactive peptides to regulate cell death by apoptosis in either a positive or negative fashion depending on the peptide and the type of target cell. The available evidence to date is strongest for the peptides endothelin, angiotensin II, vasoactive intestinal peptide, atrial natriuretic peptide, and adrenomedullin. Each of these peptides is discussed, with specific regard to apoptosis, in terms of regulatory activity, target cell specificity, and potential role in pulmonary physiology.
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Ahrén, Bo. "Regulatory peptides in the thyroid gland — a review on their localization and function." Acta Endocrinologica 124, no. 3 (March 1991): 225–32. http://dx.doi.org/10.1530/acta.0.1240225.
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Abstract. It has been demonstrated that nerve fibres storing immunoreactivity of vasoactive intestinal polypeptide, peptide histidine iso-leucine, neuropeptide Y, substance P, calcitonin gene-related peptide, galanin, and cholecystokinin exists in the thyroid, though the content of these neuropeptides is lower in the thyroid than in other organs, like in the gut. Furthermore, the parafollicular C-cells have been shown to harbour several different peptides: calcitonin, somatostatin, calcitonin gene-related peptide, gastrin-releasing peptide, katacalcin and helodermin. In addition, other regulatory peptides like atrial natriuretic hormone, growth factors, and cytokines are also produced in the thyroid. This review summarizes today's knowledge on the effects of these peptides on thyroid hormone secretion and their possible role in thyroid physiology. So far, functional studies have failed to establish any convincing effect of substance P, calcitonin gene-related peptide, galanin and cholecystokinin on basal or TSH-stimulated thyroid hormone secretion. In contrast, vasoactive intestinal peptide has convincingly been demonstrated to stimulate thyroid hormone secretion, and neuropeptide Y to potentiate the inhibitory action of noradrenaline on TSH-induced thyroid hormone secretion. This suggests that these two neuropeptides are involved in the intrathyroidal neural regulation of thyroid function. Moreover, the C-cell peptides somatostatin, calcitonin, calcitonin gene-related peptide, and katacalcin seem to be involved as inhibitors of thyroid hormone secretion, whereas both gastrin-releasing peptide and helodermin stimulate thyroid hormone secretion. Atrial natriuretic hormone and growth factors, and cytokines seem to inhibit thyroid hormone secretion. Hence, studies undertaken so far suggest a local intrathyroidal peptidergic regulatory concept, the exact role of which remains to be established.
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Spinelli, Valentina, Laura Sartiani, Alessandro Mugelli, Maria Novella Romanelli, and Elisabetta Cerbai. "Hyperpolarization-activated cyclic-nucleotide-gated channels: pathophysiological, developmental, and pharmacological insights into their function in cellular excitability." Canadian Journal of Physiology and Pharmacology 96, no. 10 (October 2018): 977–84. http://dx.doi.org/10.1139/cjpp-2018-0115.
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The hyperpolarization-activated cyclic-nucleotide-gated (HCN) proteins are voltage-dependent ion channels, conducting both Na+ and K+, blocked by millimolar concentrations of extracellular Cs+ and modulated by cyclic nucleotides (mainly cAMP) that contribute crucially to the pacemaker activity in cardiac nodal cells and subsidiary pacemakers. Over the last decades, much attention has focused on HCN current, If, in non-pacemaker cardiac cells and its potential role in triggering arrhythmias. In fact, in addition to pacemakers, HCN current is constitutively present in the human atria and has long been proposed to sustain atrial arrhythmias associated to different cardiac pathologies or triggered by various modulatory signals (catecholamines, serotonin, natriuretic peptides). An atypical If occurs in diseased ventricular cardiomyocytes, its amplitude being linearly related to the severity of cardiac hypertrophy. The properties of atrial and ventricular If and its modulation by pharmacological interventions has been object of intense study, including the synthesis and characterization of new compounds able to block preferentially HCN1, HCN2, or HCN4 isoforms. Altogether, clues emerge for opportunities of future pharmacological strategies exploiting the unique properties of this channel family: the prevalence of different HCN subtypes in organs and tissues, the possibility to target HCN gain- or loss-of-function associated with disease, the feasibility of novel isoform-selective drugs, as well as the discovery of HCN-mediated effects for old medicines.
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Ferguson, Alastair V. "The area postrema: a cardiovascular control centre at the blood-brain interface?" Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 1026–34. http://dx.doi.org/10.1139/y91-153.
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The area postrema (AP) is one of the circumventricular organs of the brain and as such it is highly vascular and lacks the normal blood-brain barrier. Anatomical tracing studies have demonstrated afferent projections to AP originating from the paraventricular nucleus, lateral parabrachial nucleus (1-PBN), nucleus tractus solitarius (NTS), as well as the vagus nerve. AP neurons have been shown to project primarily to 1-PBN, and NTS. Receptor localization studies have reported dense aggregations of many specific peptide receptors in AP including those for angiotensin II (ANG), atrial natriuretic peptide (ANP), and endothelin (ET). Electrical stimulation studies have shown that activation of AP neurons at low frequencies (<15 Hz) results in decreases in blood pressure and heart rate, while higher frequency (>20 Hz) stimulation causes increases in blood pressure. These low frequency effects on blood pressure and heart rate appear to result from activation of separate components of the autonomic nervous system. Extracellular single unit recordings have identified two functionally separate populations of AP neurons: one responsive to circulating ANG and a second apparently responsive to changes in blood pressure. In addition, AP neurons are activated by increases in circulating ET. Afferent inputs to AP neurons from 1-PBN have separate excitatory (12% of AP neurons) or inhibitory (12% of AP neurons) effects on a relatively small proportion of AP neurons. In contrast, preliminary evidence suggests a much more broadly distributed excitatory input to approximately 70% of tested AP neurons originating from the aortic depressor nerve. These studies provide considerable evidence implicating the AP as a significant neural structure regulating the cardiovascular system.Key words: circumventricular organs, nucleus tractus solitarius, cardiovascular, angiotensin, endothelin, peptides.
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Dodd-o, Jeffrey M., Maria L. Hristopoulos, Kathleen Kibler, Jolanta Gutkowska, Suhayla Mukaddam-Daher, Alfredo Gonzalez, Laura E. Welsh-Servinsky, and David B. Pearse. "The role of natriuretic peptide receptor-A signaling in unilateral lung ischemia-reperfusion injury in the intact mouse." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 4 (April 2008): L714—L723. http://dx.doi.org/10.1152/ajplung.00185.2007.
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Ischemia-reperfusion (IR) causes human lung injury in association with the release of atrial and brain natriuretic peptides (ANP and BNP), but the role of ANP/BNP in IR lung injury is unknown. ANP and BNP bind to natriuretic peptide receptor-A (NPR-A) generating cGMP and to NPR-C, a clearance receptor that can decrease intracellular cAMP. To determine the role of NPR-A signaling in IR lung injury, we administered the NPR-A blocker anantin in an in vivo SWR mouse preparation of unilateral lung IR. With uninterrupted ventilation, the left pulmonary artery was occluded for 30 min and then reperfused for 60 or 150 min. Anantin administration decreased IR-induced Evans blue dye extravasation and wet weight in the reperfused left lung, suggesting an injurious role for NPR-A signaling in lung IR. In isolated mouse lungs, exogenous ANP (2.5 nM) added to the perfusate significantly increased the filtration coefficient sevenfold only if lungs were subjected to IR. This effect of ANP was also blocked by anantin. Unilateral in vivo IR increased endogenous plasma ANP, lung cGMP concentration, and lung protein kinase G (PKGI) activation. Anantin enhanced plasma ANP concentrations and attenuated the increase in cGMP and PKGI activation but had no effect on lung cAMP. These data suggest that lung IR triggered ANP release and altered endothelial signaling so that NPR-A activation caused increased pulmonary endothelial permeability.
Dissertations / Theses on the topic "Atrial natriuretic peptides; Respiratory organs – Physiology"
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Homan, Sean David Robert. "Endogenous atrial natriuretic factor and airway control." Thesis, 1996. http://hdl.handle.net/2440/109768.
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ix, 82 leaves : ill. ; 30 cm.This thesis describes two experiments investigating the role of endogenous atrial natriuretic factor (ANF) in the modulation of airway calibre and bronchial hyperresponsiveness in humans under normal physiological conditions. Two approaches are used. One approach examines the diurnal variation of endogenous ANF and its effect on the airway function of asthmatics and non-asthmatics. The second approach analyses a change in bronchoresponsiveness and/or airway calibre in response to manipulation of endogenous ANF levels.
Thesis (M.Sc.) -- University of Adelaide, Dept. of Physiology, 1997.