Endothelin and angiotensin il-induced contraction of the rat tail artery - pharmacology of the signalling pathways

Research output: Contribution to journalArticle

Abstract

Angiotensin II (All) mediates vasoconstriction via the activation of All receptors (predominately ATI A subtype) on vascular smooth muscle cells. However, a role for All-mediated endothelin (ET-1) release from endothelial cells has been suggested from studies with the rat tail artery preparation. We have determined the contractile effects of All and ET-1 in endotheliumintact and denuded ring preparations from the rat tail artery as well as freshly dispersed single smooth muscle cells from the same tissue. Our data indicate that: (i) the contractile effects of All and ET-1 are endothelium-independent and are antagonized respectively by losartan and BQ-123, the AT, and ETA selective antagonists; (ii) The All-mediated response is dependent on intracellular Ca2+ release-whereas that of ET-1 was primarily dependent on extracellular Ca2+ entry, and can thus be pharmacologically distinguished by the use of caffeine and nifedipine respectively. These data indicate that All and ET-1 utilize distinct signalling pathways in the rat tail artery, and that the response to All does not involve ET-1 release from the endothe-lium.

Original languageEnglish
Pages (from-to)143
Number of pages1
JournalProceedings of the Western Pharmacology Society
Volume42
Publication statusPublished - 1999
Externally publishedYes

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Endothelins
Angiotensins
Tail
Arteries
Pharmacology
Smooth Muscle Myocytes
Losartan
Endothelin-1
Nifedipine
Caffeine
Vasoconstriction
Vascular Smooth Muscle
Angiotensin II
Endothelium
Endothelial Cells

ASJC Scopus subject areas

  • Pharmacology

Cite this

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title = "Endothelin and angiotensin il-induced contraction of the rat tail artery - pharmacology of the signalling pathways",
abstract = "Angiotensin II (All) mediates vasoconstriction via the activation of All receptors (predominately ATI A subtype) on vascular smooth muscle cells. However, a role for All-mediated endothelin (ET-1) release from endothelial cells has been suggested from studies with the rat tail artery preparation. We have determined the contractile effects of All and ET-1 in endotheliumintact and denuded ring preparations from the rat tail artery as well as freshly dispersed single smooth muscle cells from the same tissue. Our data indicate that: (i) the contractile effects of All and ET-1 are endothelium-independent and are antagonized respectively by losartan and BQ-123, the AT, and ETA selective antagonists; (ii) The All-mediated response is dependent on intracellular Ca2+ release-whereas that of ET-1 was primarily dependent on extracellular Ca2+ entry, and can thus be pharmacologically distinguished by the use of caffeine and nifedipine respectively. These data indicate that All and ET-1 utilize distinct signalling pathways in the rat tail artery, and that the response to All does not involve ET-1 release from the endothe-lium.",
author = "Christopher Triggle and Y. Jiang",
year = "1999",
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journal = "Proceedings of the Western Pharmacology Society",
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T1 - Endothelin and angiotensin il-induced contraction of the rat tail artery - pharmacology of the signalling pathways

AU - Triggle, Christopher

AU - Jiang, Y.

PY - 1999

Y1 - 1999

N2 - Angiotensin II (All) mediates vasoconstriction via the activation of All receptors (predominately ATI A subtype) on vascular smooth muscle cells. However, a role for All-mediated endothelin (ET-1) release from endothelial cells has been suggested from studies with the rat tail artery preparation. We have determined the contractile effects of All and ET-1 in endotheliumintact and denuded ring preparations from the rat tail artery as well as freshly dispersed single smooth muscle cells from the same tissue. Our data indicate that: (i) the contractile effects of All and ET-1 are endothelium-independent and are antagonized respectively by losartan and BQ-123, the AT, and ETA selective antagonists; (ii) The All-mediated response is dependent on intracellular Ca2+ release-whereas that of ET-1 was primarily dependent on extracellular Ca2+ entry, and can thus be pharmacologically distinguished by the use of caffeine and nifedipine respectively. These data indicate that All and ET-1 utilize distinct signalling pathways in the rat tail artery, and that the response to All does not involve ET-1 release from the endothe-lium.

AB - Angiotensin II (All) mediates vasoconstriction via the activation of All receptors (predominately ATI A subtype) on vascular smooth muscle cells. However, a role for All-mediated endothelin (ET-1) release from endothelial cells has been suggested from studies with the rat tail artery preparation. We have determined the contractile effects of All and ET-1 in endotheliumintact and denuded ring preparations from the rat tail artery as well as freshly dispersed single smooth muscle cells from the same tissue. Our data indicate that: (i) the contractile effects of All and ET-1 are endothelium-independent and are antagonized respectively by losartan and BQ-123, the AT, and ETA selective antagonists; (ii) The All-mediated response is dependent on intracellular Ca2+ release-whereas that of ET-1 was primarily dependent on extracellular Ca2+ entry, and can thus be pharmacologically distinguished by the use of caffeine and nifedipine respectively. These data indicate that All and ET-1 utilize distinct signalling pathways in the rat tail artery, and that the response to All does not involve ET-1 release from the endothe-lium.

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