Role of the hypothalamus in the control of atrial natriuretic peptide release.

Baldissera, Sandro; Menani, José Vanderlei; Santos, Lucas Felipe dos; Favaretto, A. L. V.; Gutkowska, Jolanta; Turrin, Marina Queiroz do Amaral; McCann, Samuel M.; Antunes‐Rodrigues, José

doi:10.1073/pnas.86.23.9621

Cited by 48 publications

(41 citation statements)

References 30 publications

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“…In view of the much larger quantities of the peptide stored in the atria, it is probable that changes in atrial release contribute to the alterations in plasma ANP observed after stimulation or ablation of the AV3V region; however, these results suggested that the dramatic changes in plasma ANP that followed these manipulations may be due to altered release of the peptide from brain structures as well as the atria and lungs (38,39). These stimulation and lesion experiments support a crucial role of the CNS in controlling ANP release.…”

Section: Brain Anpergic Neuronal System and Release Of Anpcontrasting

confidence: 50%

“…Therefore, we evaluated the possible role of brain ANP in evoking the changes in renal sodium excretion that followed stimulations or lesions of the AV3V, a region further implicated in control of sodium excretion by later experiments (37). Injection of carbachol into the AV3V produced the expected natriuresis on the basis of our earlier experiments, which was accompanied by a dramatic rise in plasma ANP concentration and a rise in ANP content in the medial basal hypothalamus, the neurohypophysis and particularly the anterior hypophysis but without alterations in the content of ANP in the lungs or the right or left atrium (38). The marked elevations in content of the peptide in the basal hypothalamus and neuro-and adenohypophysis suggested that the natriuresis resulting from this stimulation is brought about at least in part by release of ANP from the brain.…”

Section: Brain Anpergic Neuronal System and Release Of Anpmentioning

confidence: 99%

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Neuroendocrine control of body fluid homeostasis

McCann

Gutkowska²,

Antunes‐Rodrigues

2003

Braz J Med Biol Res

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Angiotensin II and atrial natriuretic peptide (ANP) play important and opposite roles in the control of water and salt intake, with angiotensin II promoting the intake of both and ANP inhibiting the intake of both. Following blood volume expansion, baroreceptor input to the brainstem induces the release of ANP within the hypothalamus that releases oxytocin (OT) that acts on its receptors in the heart to cause the release of ANP. ANP activates guanylyl cyclase that converts guanosine triphosphate into cyclic guanosine monophosphate (cGMP). cGMP activates protein kinase G that reduces heart rate and force of contraction, decreasing cardiac output. ANP acts similarly to induce vasodilation. The intrinsic OT system in the heart and vascular system augments the effects of circulating OT to cause a rapid reduction in effective circulating blood volume. Furthermore, natriuresis is rapidly induced by the action of ANP on its tubular guanylyl cyclase receptors, resulting in the production of cGMP that closes Na + channels. The OT released by volume expansion also acts on its tubular receptors to activate nitric oxide synthase. The nitric oxide released activates guanylyl cyclase leading to the production of cGMP that also closes Na + channels, thereby augmenting the natriuretic effect of ANP. The natriuresis induced by cGMP finally causes blood volume to return to normal. At the same time, the ANP released acts centrally to decrease water and salt intake.

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Section: Brain Anpergic Neuronal System and Release Of Anpcontrasting

confidence: 50%

Section: Brain Anpergic Neuronal System and Release Of Anpmentioning

confidence: 99%

Neuroendocrine control of body fluid homeostasis

McCann

Gutkowska²,

Antunes‐Rodrigues

2003

Braz J Med Biol Res

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“…20 Electrical stimulation of the rostral nucleus tractus solitarius raises the pANF concentration, 21 and stimulation of the region anteroventral to the third ventricle (AV3V) with carbachol produces a dramatic rise in circulating ANF levels. 22 In humans, the pANF concentration is elevated following SAH 9 -11 and intracerebral hematoma.…”

Section: Discussionmentioning

confidence: 99%

Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Diringer

Lim

Kirsch

et al. 1991

Stroke

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Following subarachnoid hemorrhage, the plasma concentration of atrial natriuretic factor is elevated and appears to be independent of atrial stretch. While the hypothalamus and circumventricular organs contribute to sodium and intravascular volume regulation, their influence on atrial natriuretic factor is not known. We tested the hypothesis that, following subarachnoid hemorrhage, suprasellar cisternal blood, intraventricular blood, or ventricular enlargement would be associated with elevated plasma levels of atrial natriuretic factor. Computed tomograms of 26 patients performed ^3 days after hemorrhage were analyzed to determine the presence of suprasellar or intraventricular blood and enlargement of the third or lateral ventricle. These results were correlated with the plasma atrial natriuretic factor and serum sodium concentrations. The initial atrial natriuretic factor concentration was elevated and was higher in patients with suprasellar or intraventricular blood than in those without (suprasellar: 131 ±20 and 54±10 pg/ml, respectively; intraventricular: 137±25 and 84±31 pg/ml, respectively). The atrial natriuretic factor concentration remained higher over the week following hemorrhage in patients with suprasellar blood than in those without (127 ±16 and 68±12 pg/ml, respectively). The atrial natriuretic factor concentration was not correlated with hyponatremia (125-134 meq/1) or age-corrected ventricular size. Hyponatremia did not correlate with the presence of intraventricular or suprasellar blood. Our data suggest that suprasellar and intraventricular blood disturb hypothalamic function, resulting in an elevated plasma atrial natriuretic factor concentration. The presence of a direct relation between atrial natriuretic factor and hyponatremia remains unclear. (Stroke 1991^22:577-581)

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“…ANP neurons (with cell bodies in the paraventricular nucleus projecting axons to the external layer of the median eminence (ME) and to the neural lobe) are important in AV3V mediated natriuresis (10). Cholinergic and adrenergic stimulation of AV3V increases sodium excretion, which is associated with a rapid increase in plasma ANP.…”

Section: Neural Control Of Hydromineral Homeostasismentioning

confidence: 99%

Oxytocin is a cardiovascular hormone

Gutkowska

Jankowski

Mukaddam‐Daher

et al. 2000

Braz J Med Biol Res

157

108

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Oxytocin (OT), a nonapeptide, was the first hormone to have its biological activities established and chemical structure determined. It was believed that OT is released from hypothalamic nerve terminals of the posterior hypophysis into the circulation where it stimulates uterine contractions during parturition, and milk ejection during lactation. However, equivalent concentrations of OT were found in the male hypophysis, and similar stimuli of OT release were determined for both sexes, suggesting other physiological functions. Indeed, recent studies indicate that OT is involved in cognition, tolerance, adaptation and complex sexual and maternal behaviour, as well as in the regulation of cardiovascular functions. It has long been known that OT induces natriuresis and causes a fall in mean arterial pressure, both after acute and chronic treatment, but the mechanism was not clear. The discovery of the natriuretic family shed new light on this matter. Atrial natriuretic peptide (ANP), a potent natriuretic and vasorelaxant hormone, originally isolated from rat atria, has been found at other sites, including the brain. Blood volume expansion causes ANP release that is believed to be important in the induction of natriuresis and diuresis, which in turn act to reduce the increase in blood volume. Neurohypophysectomy totally abolishes the ANP response to volume expansion. This indicates that one of the major hypophyseal peptides is responsible for ANP release. The role of ANP in OT-induced natriuresis was evaluated, and we hypothesized that the cardio-renal effects of OT are mediated by the release of ANP from the heart. To support this hypothesis, we have demonstrated the presence and synthesis of OT receptors in all heart compartments and the vasculature. The functionality of these receptors has been established by the ability of OT to induce ANP release from perfused heart or atrial slices. Furthermore, we have shown that the heart and large vessels like the aorta and vena cava are sites of OT synthesis. Therefore, locally produced OT may have important regulatory functions within the heart and vascular beds. Such functions may include slowing down of the heart or the regulation of local vascular tone. Correspondence

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Role of the hypothalamus in the control of atrial natriuretic peptide release.

Cited by 48 publications

References 30 publications

Neuroendocrine control of body fluid homeostasis

Neuroendocrine control of body fluid homeostasis

Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Oxytocin is a cardiovascular hormone

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