Action of C-type natriuretic peptide in isolated canine arteries and veins

C. M. Wei, L. L. Aarhus, Virginia M Miller, John C Jr. Burnett

Research output: Contribution to journalArticle

129 Citations (Scopus)

Abstract

C-type natriuretic peptide (CNP) is a hormone that shares structural homology to atrial natriuretic peptide (ANP); however, distinct receptors have been found for each in cultured aortic endothelial and smooth muscle cells. CNP in vivo reduces arterial pressure, atrial pressures, and cardiac output. These actions are consistent with a decrease in cardiac preload. Therefore, the current studies were designed to test the hypothesis that CNP is a vasodilator distinct from ANP. Rings of canine renal and saphenous arteries and renal, saphenous, and femoral veins with and without endothelium were suspended to measure isometric force in an organ chamber. CNP caused significant concentration-dependent relaxations in veins with and without endothelium contracted with phenylephrine (10-6 log M). In marked contrast, ANP caused no significant relaxation in veins either with or without endothelium. In arterial rings, responses to the peptides were heterogeneous. ANP caused relaxation in renal but not saphenous arteries. CNP induced modest and comparable relaxation in rings of saphenous but not renal arteries with and without endothelium. These results demonstrate that: 1) CNP and not ANP is a relaxing factor of isolated peripheral canine veins, and 2) the responses of arteries to ANP and CNP are heterogeneous. These findings support a distinct biological role for CNP in the regulation of cardiovascular tone.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume264
Issue number1 33-1
StatePublished - 1993

Fingerprint

C-Type Natriuretic Peptide
Canidae
Veins
Atrial Natriuretic Factor
Arteries
Endothelium
Renal Artery
Renal Veins
Atrial Pressure
Femoral Vein
Saphenous Vein
Phenylephrine
Vasodilator Agents
Cardiac Output
Smooth Muscle Myocytes
Arterial Pressure
Hormones
Kidney
Peptides

Keywords

  • atrial natriuretic peptide
  • femoral veins
  • renal arteries
  • renal veins
  • saphenous arteries

ASJC Scopus subject areas

  • Physiology

Cite this

@article{33f0fb2d1df64ad38583f8923683ca80,
title = "Action of C-type natriuretic peptide in isolated canine arteries and veins",
abstract = "C-type natriuretic peptide (CNP) is a hormone that shares structural homology to atrial natriuretic peptide (ANP); however, distinct receptors have been found for each in cultured aortic endothelial and smooth muscle cells. CNP in vivo reduces arterial pressure, atrial pressures, and cardiac output. These actions are consistent with a decrease in cardiac preload. Therefore, the current studies were designed to test the hypothesis that CNP is a vasodilator distinct from ANP. Rings of canine renal and saphenous arteries and renal, saphenous, and femoral veins with and without endothelium were suspended to measure isometric force in an organ chamber. CNP caused significant concentration-dependent relaxations in veins with and without endothelium contracted with phenylephrine (10-6 log M). In marked contrast, ANP caused no significant relaxation in veins either with or without endothelium. In arterial rings, responses to the peptides were heterogeneous. ANP caused relaxation in renal but not saphenous arteries. CNP induced modest and comparable relaxation in rings of saphenous but not renal arteries with and without endothelium. These results demonstrate that: 1) CNP and not ANP is a relaxing factor of isolated peripheral canine veins, and 2) the responses of arteries to ANP and CNP are heterogeneous. These findings support a distinct biological role for CNP in the regulation of cardiovascular tone.",
keywords = "atrial natriuretic peptide, femoral veins, renal arteries, renal veins, saphenous arteries",
author = "Wei, {C. M.} and Aarhus, {L. L.} and Miller, {Virginia M} and Burnett, {John C Jr.}",
year = "1993",
language = "English (US)",
volume = "264",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "1 33-1",

}

TY - JOUR

T1 - Action of C-type natriuretic peptide in isolated canine arteries and veins

AU - Wei, C. M.

AU - Aarhus, L. L.

AU - Miller, Virginia M

AU - Burnett, John C Jr.

PY - 1993

Y1 - 1993

N2 - C-type natriuretic peptide (CNP) is a hormone that shares structural homology to atrial natriuretic peptide (ANP); however, distinct receptors have been found for each in cultured aortic endothelial and smooth muscle cells. CNP in vivo reduces arterial pressure, atrial pressures, and cardiac output. These actions are consistent with a decrease in cardiac preload. Therefore, the current studies were designed to test the hypothesis that CNP is a vasodilator distinct from ANP. Rings of canine renal and saphenous arteries and renal, saphenous, and femoral veins with and without endothelium were suspended to measure isometric force in an organ chamber. CNP caused significant concentration-dependent relaxations in veins with and without endothelium contracted with phenylephrine (10-6 log M). In marked contrast, ANP caused no significant relaxation in veins either with or without endothelium. In arterial rings, responses to the peptides were heterogeneous. ANP caused relaxation in renal but not saphenous arteries. CNP induced modest and comparable relaxation in rings of saphenous but not renal arteries with and without endothelium. These results demonstrate that: 1) CNP and not ANP is a relaxing factor of isolated peripheral canine veins, and 2) the responses of arteries to ANP and CNP are heterogeneous. These findings support a distinct biological role for CNP in the regulation of cardiovascular tone.

AB - C-type natriuretic peptide (CNP) is a hormone that shares structural homology to atrial natriuretic peptide (ANP); however, distinct receptors have been found for each in cultured aortic endothelial and smooth muscle cells. CNP in vivo reduces arterial pressure, atrial pressures, and cardiac output. These actions are consistent with a decrease in cardiac preload. Therefore, the current studies were designed to test the hypothesis that CNP is a vasodilator distinct from ANP. Rings of canine renal and saphenous arteries and renal, saphenous, and femoral veins with and without endothelium were suspended to measure isometric force in an organ chamber. CNP caused significant concentration-dependent relaxations in veins with and without endothelium contracted with phenylephrine (10-6 log M). In marked contrast, ANP caused no significant relaxation in veins either with or without endothelium. In arterial rings, responses to the peptides were heterogeneous. ANP caused relaxation in renal but not saphenous arteries. CNP induced modest and comparable relaxation in rings of saphenous but not renal arteries with and without endothelium. These results demonstrate that: 1) CNP and not ANP is a relaxing factor of isolated peripheral canine veins, and 2) the responses of arteries to ANP and CNP are heterogeneous. These findings support a distinct biological role for CNP in the regulation of cardiovascular tone.

KW - atrial natriuretic peptide

KW - femoral veins

KW - renal arteries

KW - renal veins

KW - saphenous arteries

UR - http://www.scopus.com/inward/record.url?scp=0027511651&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027511651&partnerID=8YFLogxK

M3 - Article

C2 - 8430863

AN - SCOPUS:0027511651

VL - 264

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

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

SN - 1931-857X

IS - 1 33-1

ER -