Biological role for the endothelin-A receptor in aortic cross-clamping

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

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

The current study was undertaken to define a biological role for the endothelin-A receptor in a clinically relevant model of altered systemic and renal function produced by suprarenal aortic cross-clamping. This model is associated with profound systemic and renal vasoconstriction, acute renal failure, and a significant increase in circulating endothelin. Studies were performed in three groups of anesthetized mongrel dogs. Group 1 (n=5) underwent aortic cross-clamping for 1 hour; group 2 (n=5) underwent aortic cross-clamping for 1 hour in the presence of BQ-123, a specific antagonist of the endothelin-A receptor; group 3 (n=4) received BQ-123 alone. The marked systemic and renal vasoconstriction associated with aortic cross-clamping in group 1 was markedly attenuated in group 2 in the presence of BQ-123. Unlike the vasoconstrictor response, BQ-123 did not attenuate the decrease in glomerular filtration rate associated with this model. Under unstimulated conditions in group 3, BQ-123 had no actions on systemic or renal hemodynamics. In conclusion, the current study demonstrates that the systemic and renal vasoconstriction associated with aortic cross-clamping are in part mediated through the interaction of endothelin and the endothelin-A receptor. This study demonstrates the functional importance of increased endogenous endothelin in the regulation of vascular tone in this pathophysiological state.

Original languageEnglish (US)
Pages (from-to)62-66
Number of pages5
JournalHypertension
Volume22
Issue number1
StatePublished - 1993

Fingerprint

Endothelin A Receptors
Constriction
Endothelins
Kidney
Vasoconstriction
Vasoconstrictor Agents
Glomerular Filtration Rate
Acute Kidney Injury
Blood Vessels
Hemodynamics
cyclo(Trp-Asp-Pro-Val-Leu)
Dogs

Keywords

  • endothelins
  • receptors, endothelin
  • renal failure, acute
  • vascular resistance

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Stingo, A. J., Clavell, A. L., Aarhus, L. L., & Burnett, J. C. J. (1993). Biological role for the endothelin-A receptor in aortic cross-clamping. Hypertension, 22(1), 62-66.

Biological role for the endothelin-A receptor in aortic cross-clamping. / Stingo, A. J.; Clavell, A. L.; Aarhus, L. L.; Burnett, John C Jr.

In: Hypertension, Vol. 22, No. 1, 1993, p. 62-66.

Research output: Contribution to journalArticle

Stingo, AJ, Clavell, AL, Aarhus, LL & Burnett, JCJ 1993, 'Biological role for the endothelin-A receptor in aortic cross-clamping', Hypertension, vol. 22, no. 1, pp. 62-66.
Stingo, A. J. ; Clavell, A. L. ; Aarhus, L. L. ; Burnett, John C Jr. / Biological role for the endothelin-A receptor in aortic cross-clamping. In: Hypertension. 1993 ; Vol. 22, No. 1. pp. 62-66.
@article{1de835b796244dd5bb15bc13f2bae608,
title = "Biological role for the endothelin-A receptor in aortic cross-clamping",
abstract = "The current study was undertaken to define a biological role for the endothelin-A receptor in a clinically relevant model of altered systemic and renal function produced by suprarenal aortic cross-clamping. This model is associated with profound systemic and renal vasoconstriction, acute renal failure, and a significant increase in circulating endothelin. Studies were performed in three groups of anesthetized mongrel dogs. Group 1 (n=5) underwent aortic cross-clamping for 1 hour; group 2 (n=5) underwent aortic cross-clamping for 1 hour in the presence of BQ-123, a specific antagonist of the endothelin-A receptor; group 3 (n=4) received BQ-123 alone. The marked systemic and renal vasoconstriction associated with aortic cross-clamping in group 1 was markedly attenuated in group 2 in the presence of BQ-123. Unlike the vasoconstrictor response, BQ-123 did not attenuate the decrease in glomerular filtration rate associated with this model. Under unstimulated conditions in group 3, BQ-123 had no actions on systemic or renal hemodynamics. In conclusion, the current study demonstrates that the systemic and renal vasoconstriction associated with aortic cross-clamping are in part mediated through the interaction of endothelin and the endothelin-A receptor. This study demonstrates the functional importance of increased endogenous endothelin in the regulation of vascular tone in this pathophysiological state.",
keywords = "endothelins, receptors, endothelin, renal failure, acute, vascular resistance",
author = "Stingo, {A. J.} and Clavell, {A. L.} and Aarhus, {L. L.} and Burnett, {John C Jr.}",
year = "1993",
language = "English (US)",
volume = "22",
pages = "62--66",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Biological role for the endothelin-A receptor in aortic cross-clamping

AU - Stingo, A. J.

AU - Clavell, A. L.

AU - Aarhus, L. L.

AU - Burnett, John C Jr.

PY - 1993

Y1 - 1993

N2 - The current study was undertaken to define a biological role for the endothelin-A receptor in a clinically relevant model of altered systemic and renal function produced by suprarenal aortic cross-clamping. This model is associated with profound systemic and renal vasoconstriction, acute renal failure, and a significant increase in circulating endothelin. Studies were performed in three groups of anesthetized mongrel dogs. Group 1 (n=5) underwent aortic cross-clamping for 1 hour; group 2 (n=5) underwent aortic cross-clamping for 1 hour in the presence of BQ-123, a specific antagonist of the endothelin-A receptor; group 3 (n=4) received BQ-123 alone. The marked systemic and renal vasoconstriction associated with aortic cross-clamping in group 1 was markedly attenuated in group 2 in the presence of BQ-123. Unlike the vasoconstrictor response, BQ-123 did not attenuate the decrease in glomerular filtration rate associated with this model. Under unstimulated conditions in group 3, BQ-123 had no actions on systemic or renal hemodynamics. In conclusion, the current study demonstrates that the systemic and renal vasoconstriction associated with aortic cross-clamping are in part mediated through the interaction of endothelin and the endothelin-A receptor. This study demonstrates the functional importance of increased endogenous endothelin in the regulation of vascular tone in this pathophysiological state.

AB - The current study was undertaken to define a biological role for the endothelin-A receptor in a clinically relevant model of altered systemic and renal function produced by suprarenal aortic cross-clamping. This model is associated with profound systemic and renal vasoconstriction, acute renal failure, and a significant increase in circulating endothelin. Studies were performed in three groups of anesthetized mongrel dogs. Group 1 (n=5) underwent aortic cross-clamping for 1 hour; group 2 (n=5) underwent aortic cross-clamping for 1 hour in the presence of BQ-123, a specific antagonist of the endothelin-A receptor; group 3 (n=4) received BQ-123 alone. The marked systemic and renal vasoconstriction associated with aortic cross-clamping in group 1 was markedly attenuated in group 2 in the presence of BQ-123. Unlike the vasoconstrictor response, BQ-123 did not attenuate the decrease in glomerular filtration rate associated with this model. Under unstimulated conditions in group 3, BQ-123 had no actions on systemic or renal hemodynamics. In conclusion, the current study demonstrates that the systemic and renal vasoconstriction associated with aortic cross-clamping are in part mediated through the interaction of endothelin and the endothelin-A receptor. This study demonstrates the functional importance of increased endogenous endothelin in the regulation of vascular tone in this pathophysiological state.

KW - endothelins

KW - receptors, endothelin

KW - renal failure, acute

KW - vascular resistance

UR - http://www.scopus.com/inward/record.url?scp=0027175489&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027175489&partnerID=8YFLogxK

M3 - Article

C2 - 8319993

AN - SCOPUS:0027175489

VL - 22

SP - 62

EP - 66

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 1

ER -