Renal sympathetic nerve activity in sodium retention of acute caval constriction

Slick, GL; DiBona, G. F.; Kaloyanides, GJ

doi:10.1152/ajplegacy.1974.226.4.925

Cited by 31 publications

(9 citation statements)

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“…Substantial evidence has accumulated which implicates sympathetic nerve activity in the antinatriuresis of TIVC occlusion (Azer, 1972;Kilcoyne and Cannon, 1971b;Slick et al, 1974;Slick et al, 1975). This is supported by our finding of a markedly increased RVR after AIVC occlusion.…”

Section: Discussionsupporting

confidence: 84%

“…Subhepatic occlusion of the AIVC did not depress cortical blood flow or depressed it only moderately. However, several other investigators found that changes in intrarenal blood flow distribution are not necessary for the development of salt retention during acute caval constriction when the microsphere technique was used for measuring intrarenal blood flow distribution (Slick et al, 1974;Crumb et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

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Effects of renal and hepatic venous congestion on renal function in the presence of low and normal cardiac output in dogs.

Priebe¹,

Heimann²,

Hedley-Whyte³

1980

Circulation Research

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We investigated the effect of acute renal vein and hepatic vein hypertension induced by partial balloon-occlusion of the abdominal inferior vena cava (AIVC-O) and the thoracic inferior vena cava (TIVC-O) on systemic and renal hemodynamics and renal function in 13 dogs anesthetized with pentobarbital. When a renal vein pressure of 13 cm H2O was induced by AIVC-O, cardiac output, stroke volume, central venous pressure, renal blood flow, and renal function (GFR, free water clearance, osmolar clearance, urine output, urinary sodium excretion, fractional sodium excretion) decreased significantly. When systemic hemodynamics were restored to control values by transfusion of autologous blood (mean of 9 ml/kg body weight) while renal vein pressure was kept elevated, renal function also was restored. A hepatic venous pressure of 13 cm H2O then was induced by TIVC-O. The effects on systemic hemodynamics and renal function were very similar to those observed during AIVC-O. When systemic hemodynamics were restored to control values by transfusion (mean of 9 ml/kg), while hepatic venous hypertension was maintained by TIVC-O, renal function also was restored. Despite significant changes in natriuresis and diuresis, intrarenal blood flow distribution, as determined by the radioactive microsphere technique, remained essentially unchanged throughout. We conclude that renal and hepatic congestion induced by partial AIVC-O and TIVC-O do not, per se, alter renal function significantly.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Effects of renal and hepatic venous congestion on renal function in the presence of low and normal cardiac output in dogs.

Priebe¹,

Heimann²,

Hedley-Whyte³

1980

Circulation Research

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“…However, several studies (2-7) have demonstrated a blunted renal response to exogenous ANF in CHF. Multiple mechanisms have been implicated in this blunted renal response to ANF in CHF including: changes in ANF receptor density (8)(9)(10), enhanced degradation and clearance of ANF (11,12), altered postreceptor signal transduction (13), activation ofcounterregulatory neurohumoral systems (14,15), and decreased renal perfusion pressure (5). These mechanisms are not mutually exclusive.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

et al. 1991

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The renal natriuretic actions of endogenous atrial natriuretic factor are enhanced by neutral endopeptidase inhibition (NEP-I). Recognizing that activation ofthe renin-angiotensin-aldosterone system in congestive heart failure (CHF) antagonizes the renal actions of atrial natriuretic factor, we hypothesized that angiotensin II antagonism with converting enzyme inhibition would potentiate the renal actions of NEP-I in CHF. To test this hypothesis, the renal responses to a specific NEP-I (SQ 28,603) were assessed in dogs with eight days of experimental CHF produced by rapid ventricular pacing. The renal natriuretic responses to NEP-I in experimental CHF were significant. In the same model of CHF, chronic angiotensin antagonism with converting enzyme inhibition potentiated both renal hemodynamic and excretory responses to NEP-I. The potentiated renal hemodynamic response included significant increases in glomerular filtration rate and filtration fraction. In the CHF group with angiotensin antagonism, an intrarenal infusion of low-dose angiotensin abolished the potentiated renal responses to NEP-I, supporting the concept that intrarenal angiotensin antagonism, rather than improved systemic hemodynamics or potentiation of other peptide systems, mediated the enhanced renal responses to NEP-I in the presence of converting enzyme inhibition. (J. Clin. Invest. 1991. 88:1636-1642

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“…We have recently reported that the increases in urinary salt and water excretion which follow acute unilateral renal denervation in the rat occur in the absence of local or systemic circulatory effects, and are related to a decrease in absolute and fractional sodium and water reabsorption in the proximal tubule (3). Others have shown that acute surgical denervation or pharmacological blockade of the kidney's sympathetic supply results in a partial reversal of the antinatriuresis and a fall in proximal fractional reabsorption in dogs previously subjected to acute caval constriction (4). Also, when renal nerve activity was reduced after stimulation of the stellate ganglion, natriuresis and diuresis were observed without significant changes in glomerular filtration rate (GFR)' (5).…”

mentioning

confidence: 99%

Effect of renal sympathetic nerve stimulation on proximal water and sodium reabsorption.

Bell-Reuss¹,

Trevino²,

Gottschalk³

1976

J. Clin. Invest.

254

115

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A B S T R A C T The renal responses to sympathetic nerve stimulation were studied in saline-expanded rats. The left kidney was partially denervated by crushing the left greater splanchnic nerve. Then the distal portion of the nerve was stimulated with square wave pulses of 0.5 ms duration, voltage twice threshold, and 1 or 2 Hz frequency while monitoring the compound action potential. Fibers with conduction speeds of 13-17 m s-' and of 0.7-1 m * s-' were identified. Only stimulation of the latter appeared to produce changes in renal Na and water excretion. Whole kidney and individual nephron studies were performed alternating control and nerve stimulation periods. Nerve stimulation produced approximately a 25% reduction of the left kidney urine volume and sodium excretion. Glomerular filtration rate and renal plasma flow remained unchanged. Right kidney Na and water excretion, glomerular filtration rate, and renal plasma flow remained constant. In the left kidney, during nerve stimulation, the tubular fluid to plasma inulin concentration ratio increased significantly in the late proximal tubule.We conclude that the antidiuresis and antinatriuresis seen during sympathetic nerve stimulation were caused by increased sodium and water reabsorption in the proximal tubule, probably mediated by the stimulation of slowly conducting unmyelinated fibers. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes.

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Renal sympathetic nerve activity in sodium retention of acute caval constriction

Cited by 31 publications

References 0 publications

Effects of renal and hepatic venous congestion on renal function in the presence of low and normal cardiac output in dogs.

Effects of renal and hepatic venous congestion on renal function in the presence of low and normal cardiac output in dogs.

Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

Effect of renal sympathetic nerve stimulation on proximal water and sodium reabsorption.

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