Role of antidiuretic activity in the inhibition of renin secretion by vasopressin in anesthetized dogs

Schwartz, Jeffrey; C, Ott; Morales, Orlando; Reid, Ian A.

doi:10.1016/0196-9781(86)90067-7

Cited by 5 publications

(2 citation statements)

References 28 publications

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“…The frequent drinking and infusion of a large saline load would act to suppress AVP to barely detectable levels. The lowered AVP levels could remove inhibition of PRA release (14,26), potentially contributing to local effects on the kidney tubular function. However, the similarity in PRA in C and Ex trials provides little support for this mechanism.…”

Section: Discussionmentioning

confidence: 99%

Increased renal tubular sodium reabsorption during exercise-induced hypervolemia in humans

Nagashima

Kavouras

et al. 2001

Journal of Applied Physiology

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We tested the hypothesis that renal tubular Na(+) reabsorption increased during the first 24 h of exercise-induced plasma volume expansion. Renal function was assessed 1 day after no-exercise control (C) or intermittent cycle ergometer exercise (Ex, 85% of peak O(2) uptake) for 2 h before and 3 h after saline loading (12.5 ml/kg over 30 min) in seven subjects. Ex reduced renal blood flow (p-aminohippurate clearance) compared with C (0.83 +/- 0.12 vs. 1.49 +/- 0.24 l/min, P < 0.05) but did not influence glomerular filtration rates (97 +/- 10 ml/min, inulin clearance). Fractional tubular reabsorption of Na(+) in the proximal tubules was higher in Ex than in C (P < 0.05). Saline loading decreased fractional tubular reabsorption of Na(+) from 99.1 +/- 0.1 to 98.7 +/- 0.1% (P < 0.05) in C but not in Ex (99.3 +/- 0.1 to 99.4 +/- 0.1%). Saline loading reduced plasma renin activity and plasma arginine vasopressin levels in C and Ex, although the magnitude of decrease was greater in C (P < 0.05). These results indicate that, during the acute phase of exercise-induced plasma volume expansion, increased tubular Na(+) reabsorption is directed primarily to the proximal tubules and is associated with a decrease in renal blood flow. In addition, saline infusion caused a smaller reduction in fluid-regulating hormones in Ex. The attenuated volume-regulatory response acts to preserve distal tubular Na(+) reabsorption during saline infusion 24 h after exercise.

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Section: Discussionmentioning

confidence: 99%

Increased renal tubular sodium reabsorption during exercise-induced hypervolemia in humans

Nagashima

Kavouras

et al. 2001

Journal of Applied Physiology

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“…The V2 receptor antagonism induced by CGP 29325 may have stimulated renin secretion and induced renal vasoconstriction, indirectly. Schwartz and coworkers (14) have shown, in anesthetized water loaded dogs, that the selective antidiuretic agonist DDAVP suppressed plasma renin activity (PRA) and that the selective vasoconstrictor agonist (PheOrnOT) and the V 1 antagonist (CGP 25838E) did not affect PRA. Thus, they concluded that the inhibition of renin secretion might be mediated by antidiuretic activity.…”

Section: Effects Of Cgp 25838e On Vasoconstrictor Responses To Avpmentioning

confidence: 99%

Renal effects of specific antagonists of arginine vasopressin in dogs.

et al. 1991

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ABSTRACT-To investigate the effects on renal hemodynamics of specific antagonists of arginine vasopressin (AVP), CGP 29325 (d(CH2)5-D-Tyr(Et)VAVP), which has both anti-vasopressor and anti-antidiuretic activities against AVP, and CGP 25838E (d(CH2)5-Tyr(Me)AVP), which has only anti-vasopressor activity, were administered to normally hydrated anesthetized dogs, and the effects on renal function were examined. The pressor response and constriction of renal and mesenteric arteries induced by AVP were dose-dependently blocked by intravenous CGP 25838E. Following intrarenal arterial administration (i.r.a.) of CGP 29325 at 3,ug/min, water diuresis occurred and urine osmolality (Uosm) decreased to less than 250 mOsm/kg. Renal blood flow (RBF), glomerular filtration rate (GFR), and urinary sodium excretion (UNaV) remained unchanged. A higher dose (10,ug/min, i.r.a.) of CGP 29325 further decreased Uosm to about 110 mOsm/kg. Although arterial blood pressure (BP), GFR and UNaV remained unchanged, RBF decreased from the control value 3.7 ± 0.35 to 2.4 ± 0.40 ml/g•min. CGP 25838E (10,ug/min, i.r.a.) had no effect on renal hemodynamics and urine formation. When administered into the mesenteric artery, CGP 25838E (10,ug/min) increased mesenteric blood flow (MBF) from 199 ± 34 to 240 ± 40 ml/min without any alteration in blood pressure. We tentatively conclude that CGP 29325, at a lower dose, exerted anti-antidiuretic effects through a specific inhibition of V2 receptors, while the higher dose of CGP 29325 altered RBF, through yet to be determined mechanisms. The vasoconstrictive activity of AVP may contribute to the regulation of mesenteric circulation, but not to renal hemodynamics, in anesthetized dogs. pressor activity, while the latter mediates antidiuretic activity. In in vitro experiments, a V2 antagonist has been shown to specifically inhibit the AVP-dependent adenylate cyclase of human and animal kidneys in a competitive manner (4). A V1 receptor antagonist inhibits AVP induced smooth muscle contraction of the rat uterus (2). Antagonists which have an in vitro high specificity for V1 and/or V2 receptors may be effective agents for treating

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