Endothelium-Dependent Relaxations in Human Arteries

THOMAS F. LÜSCHER; JOHN P. COOKE; DONALD S. HOUSTON; RICARDO J. NEVES; PAUL M. VANHOUTTE

doi:10.1016/S0025-6196(12)62299-X

Endothelium-Dependent Relaxations in Human Arteries

THOMAS F. LÜSCHER, JOHN P. COOKE, DONALD S. HOUSTON, RICARDO J. NEVES, PAUL M. VANHOUTTE

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Abstract

Experiments were designed to study endothelium-dependent relaxations in human renal arteries (N = 13) and peripheral arteries (N = 8) suspended in organ chambers for isometric tension recording. In contracted arterial rings, acetylcholine caused endothelium-dependent relaxations that were not inhibited by indomethacin in either artery but were significantly augmented in the renal artery. Adenosine diphosphate and thrombin caused endothelium-dependent relaxations in renal but not in peripheral arteries. This finding suggests a heterogeneity of endothelium-dependent relaxations in human arteries and indicates that the relaxations are mediated by the release of an endothelium-derived relaxing factor (or factors) rather than the release of prostacyclin.

Original language	English (US)
Pages (from-to)	601-606
Number of pages	6
Journal	Mayo Clinic Proceedings
Volume	62
Issue number	7
DOIs	https://doi.org/10.1016/S0025-6196(12)62299-X
State	Published - 1987

ASJC Scopus subject areas

General Medicine

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title = "Endothelium-Dependent Relaxations in Human Arteries",

abstract = "Experiments were designed to study endothelium-dependent relaxations in human renal arteries (N = 13) and peripheral arteries (N = 8) suspended in organ chambers for isometric tension recording. In contracted arterial rings, acetylcholine caused endothelium-dependent relaxations that were not inhibited by indomethacin in either artery but were significantly augmented in the renal artery. Adenosine diphosphate and thrombin caused endothelium-dependent relaxations in renal but not in peripheral arteries. This finding suggests a heterogeneity of endothelium-dependent relaxations in human arteries and indicates that the relaxations are mediated by the release of an endothelium-derived relaxing factor (or factors) rather than the release of prostacyclin.",

author = "L{\"U}SCHER, {THOMAS F.} and COOKE, {JOHN P.} and HOUSTON, {DONALD S.} and NEVES, {RICARDO J.} and VANHOUTTE, {PAUL M.}",

note = "Funding Information: This study was supported in part by a grant from the Swiss National Foundation for the Advancement of Scientific Research. ",

year = "1987",

doi = "10.1016/S0025-6196(12)62299-X",

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T1 - Endothelium-Dependent Relaxations in Human Arteries

AU - LÜSCHER, THOMAS F.

AU - COOKE, JOHN P.

AU - HOUSTON, DONALD S.

AU - NEVES, RICARDO J.

AU - VANHOUTTE, PAUL M.

N1 - Funding Information: This study was supported in part by a grant from the Swiss National Foundation for the Advancement of Scientific Research.

PY - 1987

Y1 - 1987

N2 - Experiments were designed to study endothelium-dependent relaxations in human renal arteries (N = 13) and peripheral arteries (N = 8) suspended in organ chambers for isometric tension recording. In contracted arterial rings, acetylcholine caused endothelium-dependent relaxations that were not inhibited by indomethacin in either artery but were significantly augmented in the renal artery. Adenosine diphosphate and thrombin caused endothelium-dependent relaxations in renal but not in peripheral arteries. This finding suggests a heterogeneity of endothelium-dependent relaxations in human arteries and indicates that the relaxations are mediated by the release of an endothelium-derived relaxing factor (or factors) rather than the release of prostacyclin.

AB - Experiments were designed to study endothelium-dependent relaxations in human renal arteries (N = 13) and peripheral arteries (N = 8) suspended in organ chambers for isometric tension recording. In contracted arterial rings, acetylcholine caused endothelium-dependent relaxations that were not inhibited by indomethacin in either artery but were significantly augmented in the renal artery. Adenosine diphosphate and thrombin caused endothelium-dependent relaxations in renal but not in peripheral arteries. This finding suggests a heterogeneity of endothelium-dependent relaxations in human arteries and indicates that the relaxations are mediated by the release of an endothelium-derived relaxing factor (or factors) rather than the release of prostacyclin.

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Endothelium-Dependent Relaxations in Human Arteries

Abstract

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