Role of the renin-angiotensin system in the control of vasopressin secretion in conscious dogs.

Brooks, Virginia L.; Keil, L. C.; Reid, Ian A.

doi:10.1161/01.res.58.6.829

Cited by 63 publications

(30 citation statements)

References 35 publications

(43 reference statements)

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“…These responses may, in turn, be mediated via corticotropin-releasing factor (CRF), vasopressin, or All, since these factors are increased by hypotension (Plotsky et al, 1985;Brooks et al, 1986; Table 3) and have been shown to increase ACTH secretion (Ramsay et al, 1978;Rivier et al, 1982). The current studies do not support a major role for All in sodium-replete animals because angiotensin II receptor blockade with saralasin did not diminish the increase in corticosteroid concentration produced by nitroprusside-induced hypotension.…”

Section: All and Acth Secretionmentioning

confidence: 59%

“…Evidence that supports this hypothesis is that saralasin and captopril have been reported to also affect the relationship between blood pressure and vasopressin secretion (Brooks et al, 1986) and between blood pressure and heart rate. This suggests that saralasin and captopril may act by blocking a common action of angiotensin II to alter baroreflex control of heart rate, ACTH, and vasopressin secretion.…”

mentioning

confidence: 85%

“…A finding that favors this hypothesis is that All causes a similar shift in the relationship between blood pressure and plasma vasopressin concentration (Brooks et al, 1986), between blood pressure and heart rate, and between blood pressure and lumbar sympathetic activity (Guo and Abboud, 1984;Schmid et al, 1985). Thus, All may act by a common mechanism to affect baroreflex control of heart rate, sympathetic activity, ACTH, and vasopressin secretion.…”

Section: All and Acth Secretionmentioning

confidence: 99%

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Interaction between angiotensin II and the baroreceptor reflex in the control of adrenocorticotropic hormone secretion and heart rate in conscious dogs.

Brooks

Reid

1986

Circulation Research

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SUMMARY The present studies were designed to examine the effect of angiotensin II on baroreflex control of adrenocorticotropic hormone secretion and heart rate in conscious dogs. Baroreflex function was assessed by examining the relationship between blood pressure and plasma corticosteroid concentration (used as an index of adrenocorticotropic hormone secretion) and between blood pressure and pulse interval (the inverse of heart rate). Blood pressure was varied by intravenous infusion of four doses (0.3, 0.6, 1.5, and 3.0 Mg/kg per min) of the vasodilator nitroprusside. Nitroprusside infusion produced an increase in plasma corticosteroid concentration and a decrease in pulse interval, both of which were linearly related to the fall in arterial blood pressure. During infusion of angiotensin II (10 ng/kg per min), however, the lines relating blood pressure to plasma corticosteroid concentration or blood pressure to pulse interval were shifted to a higher pressure level, suggesting that angiotensin II resets the baroreceptor reflex Angiotensin II blockade with saralasm, an angiotensin II antagonist, or with captopril, a converting enzyme inhibitor, in sodium-depleted dogs with elevated plasma angiotensin II levels produced a shift m the opposite direction in these relationships Because baroreflex function in sodium-depleted dogs before angiotensin II blockade was similar to that in sodium-replete dogs, despite the increased plasma angiotensin II levels, and because treatment of sodium-replete dogs with saralasin did not affect baroreflex function, these results suggest that endogenous angiotensin II is necessary for the maintenance of normal baroreflex control of adrenocorticotropic hormone secretion and heart rate during sodium depletion. Previous studies designed to evaluate the physiological significance of angiotensin II in the control of adrenocorticotropic hormone secretion showed that high, perhaps supraphysiological, levels of exogenous angiotensin II are required to increase adrenocorticotropic hormone secretion. An additional finding of the present study was that exogenous angiotensin II produces a larger increase in adrenocorticotropic hormone secretion when the pressor effect of angiotensin II was eliminated with simultaneous infusion of the vasodilators nitroprusside or hydralazine This result suggests that experiments that evaluate the physiological role of angiotensin II in the control of adrenocorticotropic hormone secretion with infusions of exogenous All may underestimate the importance of endogenously produced angiotensin II, which is normally released without an increase in pressure. (Circ Res 58: 816-828, 1986)

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Section: All and Acth Secretionmentioning

confidence: 59%

mentioning

confidence: 85%

Section: All and Acth Secretionmentioning

confidence: 99%

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Interaction between angiotensin II and the baroreceptor reflex in the control of adrenocorticotropic hormone secretion and heart rate in conscious dogs.

Brooks

Reid

1986

Circulation Research

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“…[94][95][96][97] In cases of sodium depletion, Ang II may be necessary for maintaining normal baroreflex control of vasopressin secretion. 98 Conversion to Ang III by aminopeptidase A may be necessary for the pressor effect by interacting with AT1 receptors. 99 Brainstem Ang II acutely alters sympathetic responses to afferent inputs and may be important for the integration of autonomic response patterns.…”

Section: The Ras In the Brainmentioning

confidence: 99%

The role of the renin—angiotensin system in the pathogenesis of intracranial aneurysms

Shoja

Agutter²,

Tubbs

et al. 2011

J Renin Angiotensin Aldosterone Syst

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Introduction: Recent work has begun to elucidate the pathogenesis of intracranial aneurysms (IA) and has shown that many genes are involved in the risk for this condition. There has also been increasing research interest in the renin-angiotensin system (RAS) in the brain and its involvement in a range of cardiovascular and neurological disorders. The possibility that the RAS is implicated in the pathogenesis of IA merits further investigation. The aim of this article is to review the literature on the pathogenesis of IA and the pathophysiological significance of the brain RAS, and to identify directions for research into their association. Methods and results:A survey of the literature in these fields shows that although factors contributing to systemic hypertension predispose to IA, a large number of genes involved in endothelial cell adhesion, smooth muscle activity, extracellular matrix dynamics and the inflammatory and immune responses are also implicated. The brain RAS has a significant role in regulating blood pressure and in maintaining cerebrovascular autoregulation, but angiotensin II receptors are also involved in the maintenance of endothelial cell and vascular smooth muscle function and in the inflammatory response in the brain. Conclusions: There is strong, albeit largely circumstantial, evidence in the literature for a relationship between the brain RAS and the formation of IA. Research on the association between polymorphisms in RAS-related genes and the incidence of unruptured and ruptured IA is indicated.

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“…The intracerebroventricular administration of ANG II was recently shown to produce increased arterial pressure with elevated secretion of arginine vasopressin (AVP) (22,23). In addition, the intracerebroventricular administration of ANP inhibited the increase in both blood pressure and AVP secretion induced by the central administration of ANG II (2,8,22,27). It was suggested that circulating ANG II can stimulate AVP secretion in addition to exerting a potent pressor effect (22,23,30).…”

mentioning

confidence: 99%

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

Matsukawa

Miyamoto

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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.2010.-We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg Ϫ1 ·min Ϫ1 ) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg Ϫ1 ·min Ϫ1 ) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure and central venous pressure (CVP). Because the elevation in blood pressure could have potentially inhibited AVP secretion via baroreceptor reflexes, the effect of ANG II on blood pressure was attenuated by the simultaneous infusion of nitroprusside. ANG II alone produced a remarkable increase in plasma AVP levels when infused with nitroprusside, whereas the simultaneous ANP intravenous infusion (10 ng·kg Ϫ1 ·min Ϫ1 ) abolished the increase in plasma AVP levels induced by ANG II when blood pressure elevation was attenuated by nitroprusside. Thus, ANG II increased AVP secretion and ANP inhibited not only basal AVP secretion but also ANG II-stimulated AVP secretion in humans. These findings support the hypothesis that circulating ANP modulates AVP secretion, in part, by antagonizing the action of circulating ANG II. atrial natriuretic peptide; baroreceptor reflex; blood pressure; vasopressin ANGIOTENSIN II (ANG II) and atrial natriuretic peptide (ANP) are known to be important regulators of the fluid balance and arterial pressure (12,22,23), and an interaction between ANG II and ANP has been observed in several organs involved in the central nervous system (12,26). The intracerebroventricular administration of ANG II was recently shown to produce increased arterial pressure with elevated secretion of arginine vasopressin (AVP) (22,23). In addition, the intracerebroventricular administration of ANP inhibited the increase in both blood pressure and AVP secretion induced by the central administration of ANG II (2,8,22,27). It was suggested that circulating ANG II can stimulate AVP secretion in addition to exerting a potent pressor effect (22,23,30). However, it is still uncertain whether circulating ANP inhibits the response of AVP to circulating ANG II.In the present study, we investigated the effect of intravenous ANP infusion on the response of plasma AVP levels to intravenously infused ANG II in humans. Because the secretion of AVP is known to be inhibited by stimulation of the baroreceptors (11, 27), the pressor effect of ANG II may counteract its direct action of promoting AVP secretion. Thus, we evaluated the interaction between ANG II and ANP on AVP secretion while the elevations in arterial pressure and central venous pressure produced by ANG II were inhibited by simultaneous infusion of nitroprusside. SUBJECTS AND METHODS SubjectsWe evaluated eight healthy male volunteers (42 Ϯ 1 yr, mean age Ϯ SE). All subjects were within 10% of their ideal body weight and were determined to be free from endocrine, me...

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Role of the renin-angiotensin system in the control of vasopressin secretion in conscious dogs.

Cited by 63 publications

References 35 publications

Interaction between angiotensin II and the baroreceptor reflex in the control of adrenocorticotropic hormone secretion and heart rate in conscious dogs.

Interaction between angiotensin II and the baroreceptor reflex in the control of adrenocorticotropic hormone secretion and heart rate in conscious dogs.

The role of the renin—angiotensin system in the pathogenesis of intracranial aneurysms

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

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