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Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo.

Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in... Experimental evidence suggests that flow-dependent dilatation of conduit arteries is mediated by nitric oxide (NO) and/or prostacyclin. The present study was designed to assess whether NO or prostacyclin also contributes to flow-dependent dilatation of conduit arteries in humans. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation Pubmed

Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo.

Joannides, R; Haefeli, W E; Linder, L; Richard, V; Bakkali, E H; Thuillez, C; Lüscher, T F
Circulation , Volume 91 (5): -1304 – Mar 24, 1995
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Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo.


Abstract

Experimental evidence suggests that flow-dependent dilatation of conduit arteries is mediated by nitric oxide (NO) and/or prostacyclin. The present study was designed to assess whether NO or prostacyclin also contributes to flow-dependent dilatation of conduit arteries in humans.

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ISSN
0009-7322
DOI
10.1161/01.cir.91.5.1314
pmid
7867167

Abstract

Experimental evidence suggests that flow-dependent dilatation of conduit arteries is mediated by nitric oxide (NO) and/or prostacyclin. The present study was designed to assess whether NO or prostacyclin also contributes to flow-dependent dilatation of conduit arteries in humans.

Journal

Circulation – Pubmed

Published: Mar 24, 1995

There are no references for this article.