Interactions Between Vasopressin and the Renin–Angiotensin System

Reid, Ian A.; Schwartz, Jeffrey; Liu, Ben; Maselli, Judy; Keil, L. C.

doi:10.1016/s0079-6123(08)64414-3

Cited by 21 publications

(13 citation statements)

References 47 publications

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“…It is known that the activity of the renin-angiotensin system is enhanced in DI rats, possibly as a means of compensating for the absence of AVP. 24 However, under the same experimental conditions as applied in the present study, Hiwatari et al 23 demonstrated that, after total autonomic blockade, blood pressure in DI rats was lower than that in LE rats, and the reninangiotensin system was activated more by autonomic blockade in the former. Therefore, higher blood pressure in DI rats may not be attributable to enhanced activity of the renin-angiotensin system.…”

Section: Discussionsupporting

confidence: 43%

Cardiovascular depression and stabilization by central vasopressin in rats.

et al. 1990

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The role of endogenous vasopressin in cardiovascular homeostasis was examined using vasopressin-deftcient rats (Brattleboro) (n=194) and their parent strain, Long-Evans rats (n=181). Mean arterial pressure (blood pressure) and heart rate were measured every 4 seconds with or without infusion of drug solution for 21 hours, and mean values and their standard deviations (lability) were calculated. Blood pressure in Brattleboro rats (116±1.1 mm Hg, mean±SEM) was significantly higher than that in Long-Evans rats (96±0.7 mm Hg, /><0.001), whereas heart rates (381±33 and 375±2.9 beats/min, respectively) were similar. The lability of blood pressure and heart rate in Brattleboro rats (9.2±0.1 mm Hg and 42 J±0.7 beats/min) was also greater than that in Long-Evans rats (6.7 ±0.1 mm Hg, p< 0.001 and 38.4±0.8 beats/min, p<0.0l, respectively). In Brattleboro rats, intravenous vasopressin (0.1 ng/kg/min or 0.6 ng/kg/min) did not affect blood pressure, although it did reduce heart rate and decreased lability of blood pressure and heart rate. Intracerebroventricular (central) infusion of vasopressin (2 pg/kg/min) in Brattleboro rats induced initial hypertension and tachycardia followed by long-lasting hypotension and bradycardia, whereas in Long-Evans rats it induced only hypertension and tachycardia. In both strains, central vasopressin dramatically decreased the lability of blood pressure and heart rate. A rginine vasopressin (AVP) has long been known to possess potent vasoconstrictor properties. 1 However, when AVP is infused intravenously into conscious animals or humans, there is no increase in blood pressure until extremely high plasma AVP levels are achieved. 2 Evidence has accumulated indicating that the absence of increases in blood pressure in response to AVP infusion in normotensive animals may be due to the presence of an effective and specific buffering system. 3 -5 On the basis of available evidence, it has been proposed that the locus of this buffering system is in the central nervous system. 6 -12 Recently, it has been reported that Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI rats) have suppressed baroreceptor reflex sensitivity. 9 Exogenous AVP and the V 2 renal receptor agonist desmopressin (DDAVP) administered systemically is able to restore this suppressed sensitivity to within the range that is normal for Long-Evans (LE) rats. 9 It is believed that the inhibition of baroreceptor reflex pathway raises blood pressure. 13 Therefore, it may be postulated that rats with suppressed baroreceptor reflex mechanisms will have higher blood pressure and heart rate and a greater lability of blood pressure and heart rate than normal rats. Furthermore, we previously reported that centrally administered AVP lowered blood pressure in DI rats as well as in stroke-prone by guest on May 11, 2018 http://hyper.ahajournals.org/ Downloaded from

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Section: Discussionsupporting

confidence: 43%

Cardiovascular depression and stabilization by central vasopressin in rats.

et al. 1990

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“…The reduction in plasma renin activity (PRA) following the infusion of VP is consistent with that observed in terrestrial mammals (Johnson et al, 1979;Merrill and Cowley, 1986;Reid et al, 1983); however, the lack of a decrease in AII was unexpected since a decrease in renin may also be associated with a decrease in AII (Morton et al, 1982). The dissociation between renin and AII in the present study suggests that (1) the production of AII is unaffected by the observed reductions in renin or (2) the reduction in AII is delayed beyond the 24·h period examined in fasting northern elephant seal pups.…”

Section: Table·1 Fractional Excretion Of Electrolytes and Urea Over supporting

confidence: 75%

Acutely elevated vasopressin increases circulating concentrations of cortisol and aldosterone in fasting northern elephant seal (Mirounga angustirostris) pups

Ortiz

Wade

Ortiz

et al. 2003

Journal of Experimental Biology

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SUMMARYThe physiological actions of vasopressin (VP) in marine mammals are not well defined. To help elucidate its hormonal and renal effects in this group of mammals, northern elephant seal (Mirounga angustirostris) pups(N=7; 99±4 kg) were first infused with 0.9% saline (control;220 ml), followed 24 h later with VP (as a 20 ng kg-1 bolus, then 2 ng kg-1 min-1 for approximately 35 min in 225±16 ml saline). During both control and VP periods, blood samples were collected prior to infusion, and 15, 30, 60, 120 min and 24 h after infusion to examine the hormonal responses of the pups to VP. Renal responses were quantified from 24 h urine samples obtained prior to infusion (control) and 24 h post-infusion. Compared to the control period, infusion of VP increased plasma concentrations of cortisol over a 120 min period and aldosterone over 30 min,while plasma renin activity (PRA) was decreased for a 120 min period. The plasma urea:creatinine ratio was elevated following infusion of VP. Urine output and osmotic clearance were increased by 69±18% (mean ± s.e.m.) and 36±10%, respectively, but free water clearance and glomerular filtration rate were not significantly altered 24 h post-infusion of VP. Solute (osmolality, Na+, K+ and Cl-) excretion and fractional excretion of electrolytes were also increased when compared to control values. The increase in cortisol concentration suggests that VP may possess corticotropin releasing hormone-like activity in elephant seals. If osmotic diuresis and natriuresis are typical consequences of elevated [VP] in fasting pups, then not increasing VP normally during the fast may serve as a protective mechanism to avoid the potential loss of Na+ induced by elevated [VP]. Therefore, under natural fasting conditions, pups may be highly sensitive to small changes in[VP], resulting in the maintenance of water and electrolyte balance.

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“…A small but significant fall in PRA levels was observed in animals with heart failure after treatment with the AVPA. This is surprising, since vasopressin is known to suppress renal renin release, although the mechanisms have not been defined (30). Moreover, the fall in blood pressure and increased NE levels after AVPA would tend to increase PRA.…”

Section: Discussionmentioning

confidence: 99%

Vasoconstrictor role for vasopressin in experimental heart failure in the rabbit.

Arnolda¹,

McGrath²,

Cocks³

et al. 1986

J. Clin. Invest.

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Vasopressin's role as a vasoconstrictor in chronic heart failure was examined in rabbits with adriamycin cardiomyopathic congestive heart failure. Chronic adriamycin treatment resulted in a decrease in cardiac output (829±38-610±36 ml/mi, P < 0.005) and blood pressure (83±2-76±3 mmHg, P < 0.01), and an increase in peripheral resistance (8,377±381-10,170±657 dyn-s-cm-, P < 0.05). Plasma renin activity (4.7±0.6-10.9±2.8 ng angiotensin I/ml * h) and norepinephrine (0.7±0.1-13±0.2 pmol/mL P < 0.05) increased while plasma vasopressin levels did not change. Vasopressin infusion, however, produced significantly greater increases in peripheral resistance in animals with heart failure than in controls. Moreover, a specific vasopressin vascular antagonist reduced blood pressure (7±3%) and peripheral resistance (14±4%) and increased cardiac output (10±3%) in animals with heart failure but had no cardiovascular effects in normal rabbits. These results suggest that vascular sensitivity to vasopressin is increased in heart failure, and that it contributes significantly to the increased afterload in heart failure despite normal plasma levels. In this model of severe, chronic heart failure the sympathetic, renin-angiotensin, and vasopressin systems all appear to be activated.

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Interactions Between Vasopressin and the Renin–Angiotensin System

Cited by 21 publications

References 47 publications

Cardiovascular depression and stabilization by central vasopressin in rats.

Cardiovascular depression and stabilization by central vasopressin in rats.

Acutely elevated vasopressin increases circulating concentrations of cortisol and aldosterone in fasting northern elephant seal (Mirounga angustirostris) pups

Vasoconstrictor role for vasopressin in experimental heart failure in the rabbit.

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