Hormonal determinants of sodium excretion in rats with experimental high-output heart failure

J. Winaver, A. Hoffman, John C Jr. Burnett, A. Haramati

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

The present study evaluates the interrelationship between the alteration in atrial natriuretic factor (ANF) and the renal handling of Na in rats with chronic aortocaval (a-v) fistula, an experimental model of congestive heart failure. Balance studies in these animals showed two distinct patterns of Na excretion: some rats developed progressive Na retention [urinary sodium excretion (U(Na)V)<100 μeq/24 h], whereas others compensated and returned to normal Na balance (U(Na)V>1,200 μeq/24 h). Base-line plasma ANF levels were equally elevated in Na-retaining and compensated rats with a-y fistula (588 ± 70 vs. 621 ± 114 pg/ml, P, NS). However, the response of the two groups to exogenous administration of synthetic rat ANF-(101-126) in incremental doses varied greatly. ANF infusion increased the fractional Na excretion (FE(Na)) in compensated animals from 0.12 ± 9.93 to 2.6 ± 0.5%, whereas the rise in FE(Na) in Na-retaining animals was markedly blunted (0.11 ± 0.06 to 0.89 ± 0.35%). A similar pattern of ANF action was observed on the glomerular filtration rate and urine flow. The blunted response to ANF in the Na-retaining animals was associated with a marked increase in plasma renin activity (PRA) (35.6 ± 6.9 vs. 4.5 ± 0.7 ng ANG I·ml-1·h-1 in sham control rats, P < 0.05) and plasma aldosterone levels (729.3 ± 28.2 vs. 42.6 ± 18.4 ng/dl in sham control rats, P < 0.05). In contrast, PRA (6.7 ± 1.1 ng ANG I·ml-1·h-1) and plasma aldosterone (34.2 ± 8.2 ng/dl) in the compensated animals did not differ from the sham control rats. Finally, chronic inhibition of converting enzyme (with enalapril) in Na-retaining rats resulted in a significant natriuresis. The data suggest that the balance between the two opposing hormonal systems, ANF and the renin-angiotensin system, is an important determinant of Na excretion in this model of heart failure and that removal of the influence of the renin-angiotensin system facilitates the expression of the natriuretic effect of ANF.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume254
Issue number5
StatePublished - 1988
Externally publishedYes

Fingerprint

Atrial Natriuretic Factor
Heart Failure
Sodium
Renin-Angiotensin System
Aldosterone
Renin
Fistula
Natriuretic Agents
Natriuresis
Enalapril
Urinary Retention
Glomerular Filtration Rate
Theoretical Models
Urine
Kidney
Enzymes

ASJC Scopus subject areas

  • Physiology

Cite this

@article{89bcd0603f6c4179bed6baa636120a0a,
title = "Hormonal determinants of sodium excretion in rats with experimental high-output heart failure",
abstract = "The present study evaluates the interrelationship between the alteration in atrial natriuretic factor (ANF) and the renal handling of Na in rats with chronic aortocaval (a-v) fistula, an experimental model of congestive heart failure. Balance studies in these animals showed two distinct patterns of Na excretion: some rats developed progressive Na retention [urinary sodium excretion (U(Na)V)<100 μeq/24 h], whereas others compensated and returned to normal Na balance (U(Na)V>1,200 μeq/24 h). Base-line plasma ANF levels were equally elevated in Na-retaining and compensated rats with a-y fistula (588 ± 70 vs. 621 ± 114 pg/ml, P, NS). However, the response of the two groups to exogenous administration of synthetic rat ANF-(101-126) in incremental doses varied greatly. ANF infusion increased the fractional Na excretion (FE(Na)) in compensated animals from 0.12 ± 9.93 to 2.6 ± 0.5{\%}, whereas the rise in FE(Na) in Na-retaining animals was markedly blunted (0.11 ± 0.06 to 0.89 ± 0.35{\%}). A similar pattern of ANF action was observed on the glomerular filtration rate and urine flow. The blunted response to ANF in the Na-retaining animals was associated with a marked increase in plasma renin activity (PRA) (35.6 ± 6.9 vs. 4.5 ± 0.7 ng ANG I·ml-1·h-1 in sham control rats, P < 0.05) and plasma aldosterone levels (729.3 ± 28.2 vs. 42.6 ± 18.4 ng/dl in sham control rats, P < 0.05). In contrast, PRA (6.7 ± 1.1 ng ANG I·ml-1·h-1) and plasma aldosterone (34.2 ± 8.2 ng/dl) in the compensated animals did not differ from the sham control rats. Finally, chronic inhibition of converting enzyme (with enalapril) in Na-retaining rats resulted in a significant natriuresis. The data suggest that the balance between the two opposing hormonal systems, ANF and the renin-angiotensin system, is an important determinant of Na excretion in this model of heart failure and that removal of the influence of the renin-angiotensin system facilitates the expression of the natriuretic effect of ANF.",
author = "J. Winaver and A. Hoffman and Burnett, {John C Jr.} and A. Haramati",
year = "1988",
language = "English (US)",
volume = "254",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Hormonal determinants of sodium excretion in rats with experimental high-output heart failure

AU - Winaver, J.

AU - Hoffman, A.

AU - Burnett, John C Jr.

AU - Haramati, A.

PY - 1988

Y1 - 1988

N2 - The present study evaluates the interrelationship between the alteration in atrial natriuretic factor (ANF) and the renal handling of Na in rats with chronic aortocaval (a-v) fistula, an experimental model of congestive heart failure. Balance studies in these animals showed two distinct patterns of Na excretion: some rats developed progressive Na retention [urinary sodium excretion (U(Na)V)<100 μeq/24 h], whereas others compensated and returned to normal Na balance (U(Na)V>1,200 μeq/24 h). Base-line plasma ANF levels were equally elevated in Na-retaining and compensated rats with a-y fistula (588 ± 70 vs. 621 ± 114 pg/ml, P, NS). However, the response of the two groups to exogenous administration of synthetic rat ANF-(101-126) in incremental doses varied greatly. ANF infusion increased the fractional Na excretion (FE(Na)) in compensated animals from 0.12 ± 9.93 to 2.6 ± 0.5%, whereas the rise in FE(Na) in Na-retaining animals was markedly blunted (0.11 ± 0.06 to 0.89 ± 0.35%). A similar pattern of ANF action was observed on the glomerular filtration rate and urine flow. The blunted response to ANF in the Na-retaining animals was associated with a marked increase in plasma renin activity (PRA) (35.6 ± 6.9 vs. 4.5 ± 0.7 ng ANG I·ml-1·h-1 in sham control rats, P < 0.05) and plasma aldosterone levels (729.3 ± 28.2 vs. 42.6 ± 18.4 ng/dl in sham control rats, P < 0.05). In contrast, PRA (6.7 ± 1.1 ng ANG I·ml-1·h-1) and plasma aldosterone (34.2 ± 8.2 ng/dl) in the compensated animals did not differ from the sham control rats. Finally, chronic inhibition of converting enzyme (with enalapril) in Na-retaining rats resulted in a significant natriuresis. The data suggest that the balance between the two opposing hormonal systems, ANF and the renin-angiotensin system, is an important determinant of Na excretion in this model of heart failure and that removal of the influence of the renin-angiotensin system facilitates the expression of the natriuretic effect of ANF.

AB - The present study evaluates the interrelationship between the alteration in atrial natriuretic factor (ANF) and the renal handling of Na in rats with chronic aortocaval (a-v) fistula, an experimental model of congestive heart failure. Balance studies in these animals showed two distinct patterns of Na excretion: some rats developed progressive Na retention [urinary sodium excretion (U(Na)V)<100 μeq/24 h], whereas others compensated and returned to normal Na balance (U(Na)V>1,200 μeq/24 h). Base-line plasma ANF levels were equally elevated in Na-retaining and compensated rats with a-y fistula (588 ± 70 vs. 621 ± 114 pg/ml, P, NS). However, the response of the two groups to exogenous administration of synthetic rat ANF-(101-126) in incremental doses varied greatly. ANF infusion increased the fractional Na excretion (FE(Na)) in compensated animals from 0.12 ± 9.93 to 2.6 ± 0.5%, whereas the rise in FE(Na) in Na-retaining animals was markedly blunted (0.11 ± 0.06 to 0.89 ± 0.35%). A similar pattern of ANF action was observed on the glomerular filtration rate and urine flow. The blunted response to ANF in the Na-retaining animals was associated with a marked increase in plasma renin activity (PRA) (35.6 ± 6.9 vs. 4.5 ± 0.7 ng ANG I·ml-1·h-1 in sham control rats, P < 0.05) and plasma aldosterone levels (729.3 ± 28.2 vs. 42.6 ± 18.4 ng/dl in sham control rats, P < 0.05). In contrast, PRA (6.7 ± 1.1 ng ANG I·ml-1·h-1) and plasma aldosterone (34.2 ± 8.2 ng/dl) in the compensated animals did not differ from the sham control rats. Finally, chronic inhibition of converting enzyme (with enalapril) in Na-retaining rats resulted in a significant natriuresis. The data suggest that the balance between the two opposing hormonal systems, ANF and the renin-angiotensin system, is an important determinant of Na excretion in this model of heart failure and that removal of the influence of the renin-angiotensin system facilitates the expression of the natriuretic effect of ANF.

UR - http://www.scopus.com/inward/record.url?scp=0023942416&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023942416&partnerID=8YFLogxK

M3 - Article

C2 - 2966592

AN - SCOPUS:0023942416

VL - 254

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 5

ER -