Biological actions of brain natriuretic peptide in thoracic inferior vena caval constriction

A. L. Clavell, A. J. Stingo, L. L. Aarhus, John C Jr. Burnett

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Brain natriuretic peptide (BNP) shares structural and functional similarities to atrial natriuretic peptide (ANP). Although BNP and ANP interact with the same biologically active guanylate cyclase-coupled receptor, recent reports conflict with regard to the biological actions of exogenous BNP in sodium-retaining and edematous states. We studied the biological actions of BNP in normal dogs (n = 5) and sodium-avid dogs with chronic thoracic inferior vena caval constriction (TIVCC) (n = 6). In normal dogs BNP increased glomerular filtration rate, renal blood flow, and urinary sodium excretion and decreased proximal and distal fractional reabsorption of sodium with activation of urinary guanosine 3',5'-cyclic monophosphate (cGMP). These renal actions occurred in association with marked hypotensive actions and activation of systemic cGMP. In TIVCC, a state characterized by chronic reductions of cardiac output, avid sodium retention, edema, and activation of the renin-angiotensin-aldosterone system (RAAS), the renal actions of BNP were absent in association with marked attenuation of the urinary cGMP response. In contrast, an enhanced hypotensive response with preserved activation of systemic cGMP was observed. In neither normal dogs nor TIVCC dogs did BNP inhibit the RAAS. These studies report that BNP is a potent vasoactive and natriuretic peptide with potent proximal and distal tubular actions in normal dogs. These studies also demonstrate that in TIVCC, a model of low cardiac output and congestive failure that results in marked sodium retention with edema in which there is activation of the RAAS, the renal actions of BNP are attenuated while the vasoactive actions are enhanced.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume265
Issue number6 34-6
StatePublished - Dec 1 1993

Fingerprint

Venae Cavae
Brain Natriuretic Peptide
Constriction
Thorax
Sodium
Dogs
Renin-Angiotensin System
Atrial Natriuretic Factor
Kidney
Edema
Guanylate Cyclase-Coupled Receptors
Low Cardiac Output
Natriuretic Peptides
Renal Circulation
Cyclic GMP
Glomerular Filtration Rate
Cardiac Output

Keywords

  • guanosine 3',5'-cyclic monophosphate
  • natriuretic peptides
  • renal sodium excretion
  • thoracic inferior vena caval constriction

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Biological actions of brain natriuretic peptide in thoracic inferior vena caval constriction. / Clavell, A. L.; Stingo, A. J.; Aarhus, L. L.; Burnett, John C Jr.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 265, No. 6 34-6, 01.12.1993.

Research output: Contribution to journalArticle

@article{d99c8d7e540245f89122a93e0ced697b,
title = "Biological actions of brain natriuretic peptide in thoracic inferior vena caval constriction",
abstract = "Brain natriuretic peptide (BNP) shares structural and functional similarities to atrial natriuretic peptide (ANP). Although BNP and ANP interact with the same biologically active guanylate cyclase-coupled receptor, recent reports conflict with regard to the biological actions of exogenous BNP in sodium-retaining and edematous states. We studied the biological actions of BNP in normal dogs (n = 5) and sodium-avid dogs with chronic thoracic inferior vena caval constriction (TIVCC) (n = 6). In normal dogs BNP increased glomerular filtration rate, renal blood flow, and urinary sodium excretion and decreased proximal and distal fractional reabsorption of sodium with activation of urinary guanosine 3',5'-cyclic monophosphate (cGMP). These renal actions occurred in association with marked hypotensive actions and activation of systemic cGMP. In TIVCC, a state characterized by chronic reductions of cardiac output, avid sodium retention, edema, and activation of the renin-angiotensin-aldosterone system (RAAS), the renal actions of BNP were absent in association with marked attenuation of the urinary cGMP response. In contrast, an enhanced hypotensive response with preserved activation of systemic cGMP was observed. In neither normal dogs nor TIVCC dogs did BNP inhibit the RAAS. These studies report that BNP is a potent vasoactive and natriuretic peptide with potent proximal and distal tubular actions in normal dogs. These studies also demonstrate that in TIVCC, a model of low cardiac output and congestive failure that results in marked sodium retention with edema in which there is activation of the RAAS, the renal actions of BNP are attenuated while the vasoactive actions are enhanced.",
keywords = "guanosine 3',5'-cyclic monophosphate, natriuretic peptides, renal sodium excretion, thoracic inferior vena caval constriction",
author = "Clavell, {A. L.} and Stingo, {A. J.} and Aarhus, {L. L.} and Burnett, {John C Jr.}",
year = "1993",
month = "12",
day = "1",
language = "English (US)",
volume = "265",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "6 34-6",

}

TY - JOUR

T1 - Biological actions of brain natriuretic peptide in thoracic inferior vena caval constriction

AU - Clavell, A. L.

AU - Stingo, A. J.

AU - Aarhus, L. L.

AU - Burnett, John C Jr.

PY - 1993/12/1

Y1 - 1993/12/1

N2 - Brain natriuretic peptide (BNP) shares structural and functional similarities to atrial natriuretic peptide (ANP). Although BNP and ANP interact with the same biologically active guanylate cyclase-coupled receptor, recent reports conflict with regard to the biological actions of exogenous BNP in sodium-retaining and edematous states. We studied the biological actions of BNP in normal dogs (n = 5) and sodium-avid dogs with chronic thoracic inferior vena caval constriction (TIVCC) (n = 6). In normal dogs BNP increased glomerular filtration rate, renal blood flow, and urinary sodium excretion and decreased proximal and distal fractional reabsorption of sodium with activation of urinary guanosine 3',5'-cyclic monophosphate (cGMP). These renal actions occurred in association with marked hypotensive actions and activation of systemic cGMP. In TIVCC, a state characterized by chronic reductions of cardiac output, avid sodium retention, edema, and activation of the renin-angiotensin-aldosterone system (RAAS), the renal actions of BNP were absent in association with marked attenuation of the urinary cGMP response. In contrast, an enhanced hypotensive response with preserved activation of systemic cGMP was observed. In neither normal dogs nor TIVCC dogs did BNP inhibit the RAAS. These studies report that BNP is a potent vasoactive and natriuretic peptide with potent proximal and distal tubular actions in normal dogs. These studies also demonstrate that in TIVCC, a model of low cardiac output and congestive failure that results in marked sodium retention with edema in which there is activation of the RAAS, the renal actions of BNP are attenuated while the vasoactive actions are enhanced.

AB - Brain natriuretic peptide (BNP) shares structural and functional similarities to atrial natriuretic peptide (ANP). Although BNP and ANP interact with the same biologically active guanylate cyclase-coupled receptor, recent reports conflict with regard to the biological actions of exogenous BNP in sodium-retaining and edematous states. We studied the biological actions of BNP in normal dogs (n = 5) and sodium-avid dogs with chronic thoracic inferior vena caval constriction (TIVCC) (n = 6). In normal dogs BNP increased glomerular filtration rate, renal blood flow, and urinary sodium excretion and decreased proximal and distal fractional reabsorption of sodium with activation of urinary guanosine 3',5'-cyclic monophosphate (cGMP). These renal actions occurred in association with marked hypotensive actions and activation of systemic cGMP. In TIVCC, a state characterized by chronic reductions of cardiac output, avid sodium retention, edema, and activation of the renin-angiotensin-aldosterone system (RAAS), the renal actions of BNP were absent in association with marked attenuation of the urinary cGMP response. In contrast, an enhanced hypotensive response with preserved activation of systemic cGMP was observed. In neither normal dogs nor TIVCC dogs did BNP inhibit the RAAS. These studies report that BNP is a potent vasoactive and natriuretic peptide with potent proximal and distal tubular actions in normal dogs. These studies also demonstrate that in TIVCC, a model of low cardiac output and congestive failure that results in marked sodium retention with edema in which there is activation of the RAAS, the renal actions of BNP are attenuated while the vasoactive actions are enhanced.

KW - guanosine 3',5'-cyclic monophosphate

KW - natriuretic peptides

KW - renal sodium excretion

KW - thoracic inferior vena caval constriction

UR - http://www.scopus.com/inward/record.url?scp=0027145766&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027145766&partnerID=8YFLogxK

M3 - Article

C2 - 8285286

AN - SCOPUS:0027145766

VL - 265

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 6 34-6

ER -