Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure

Debra L. Fett, Patricia G. Cavero, John C Jr. Burnett

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2(N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

Original languageEnglish (US)
Pages (from-to)162-167
Number of pages6
JournalJournal of the American Society of Nephrology
Volume4
Issue number2
StatePublished - Aug 1993

Fingerprint

Furosemide
Atrial Natriuretic Factor
Renin-Angiotensin System
Heart Failure
Natriuresis
Sodium
Control Groups
Hypotension
Theoretical Models
Maintenance
Dogs

Keywords

  • Congestive heart failure
  • Diuretics
  • Natriuretic peptides

ASJC Scopus subject areas

  • Nephrology

Cite this

Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure. / Fett, Debra L.; Cavero, Patricia G.; Burnett, John C Jr.

In: Journal of the American Society of Nephrology, Vol. 4, No. 2, 08.1993, p. 162-167.

Research output: Contribution to journalArticle

@article{115ddca409244a598059e3b597cddeff,
title = "Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure",
abstract = "This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2(N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.",
keywords = "Congestive heart failure, Diuretics, Natriuretic peptides",
author = "Fett, {Debra L.} and Cavero, {Patricia G.} and Burnett, {John C Jr.}",
year = "1993",
month = "8",
language = "English (US)",
volume = "4",
pages = "162--167",
journal = "Journal of the American Society of Nephrology : JASN",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "2",

}

TY - JOUR

T1 - Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure

AU - Fett, Debra L.

AU - Cavero, Patricia G.

AU - Burnett, John C Jr.

PY - 1993/8

Y1 - 1993/8

N2 - This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2(N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

AB - This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2(N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

KW - Congestive heart failure

KW - Diuretics

KW - Natriuretic peptides

UR - http://www.scopus.com/inward/record.url?scp=0027649890&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027649890&partnerID=8YFLogxK

M3 - Article

C2 - 8400079

AN - SCOPUS:0027649890

VL - 4

SP - 162

EP - 167

JO - Journal of the American Society of Nephrology : JASN

JF - Journal of the American Society of Nephrology : JASN

SN - 1046-6673

IS - 2

ER -