The vasodilator potency of the endothelium-derived relaxing factor, l- S-nitrosocysteine, is impaired in conscious spontaneously hypertensive rats

Stephen J. Lewis; Maleka P. Hashmi-Hill; Joy R. Owen; Kevin Sandock; Tom P. Robertson; James N. Bates

doi:10.1016/j.vph.2006.03.013

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The vasodilator potency of the endothelium-derived relaxing factor, l- S-nitrosocysteine, is impaired in conscious spontaneously hypertensive rats

Journal article

Peer reviewed

The vasodilator potency of the endothelium-derived relaxing factor, l- S-nitrosocysteine, is impaired in conscious spontaneously hypertensive rats

Stephen J. Lewis, Maleka P. Hashmi-Hill, Joy R. Owen, Kevin Sandock, Tom P. Robertson and James N. Bates

Vascular pharmacology, Vol.44(6), pp.476-490

06/01/2006

DOI: 10.1016/j.vph.2006.03.013

PMID: 16697269

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Abstract

Objective This study compared the hemodynamic responses elicited by the endothelium-derived relaxing factor (EDRF), l-S-nitrosocysteine (l-SNC), the non-prostanoid EDRF released by acetylcholine (ACh) and nitric oxide (NO)-donors such as MAHMA NONOate, in conscious spontaneously hypertensive (SH) and normotensive Wistar–Kyoto (WKY) rats. Methods The depressor and/or vasodilator responses elicited by intravenous injections of ACh, l-SNC and MAHMA NONOate were determined in adult WKY and SH rats before and after intravenous injection of the NO synthesis inhibitor, NG-nitro-l-arginine methylester (l-NAME), or the cyclooxygenase inhibitor, indomethacin. Results The responses elicited by ACh and l-SNC were smaller in SH than in WKY rats whereas the responses elicited by MAHMA NONOate were augmented in SH rats. The ACh-induced responses were not diminished after injection of l-NAME in WKY or SH rats. Indomethacin did not affect the responses to any of the vasodilator agents in WKY or SH rats. Addition of l-SNC to whole blood or thoracic aortae from SH rats yielded similar amounts of NO to those of WKY rats. Conclusions The vasodilator potencies of ACh and l-SNC were diminished whereas that of NO was augmented in SH rats. The loss of potency of l-SNC in SH rats was not obviously due to differences in decomposition to NO or the overactivity of cyclooxygenase factors. This study provides the first evidence that diminished endothelium-dependent vasodilation in SH rats may involve a loss of vasodilator potency of endogenous l-SNC.

Hemodynamics

Cyclooxygenase

Nitric oxide

S-Nitrosothiols

Spontaneously hypertensive rats (SHR)

Wistar–Kyoto rats (WKY)

Details

Title: Subtitle: The vasodilator potency of the endothelium-derived relaxing factor, l- S-nitrosocysteine, is impaired in conscious spontaneously hypertensive rats
Creators: Stephen J. Lewis - Case Western Reserve University
Maleka P. Hashmi-Hill - Department of Physiology and Pharmacology, Institute of Comparative Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389, USA
Joy R. Owen - University of Georgia
Kevin Sandock - Department of Physiology and Pharmacology, Institute of Comparative Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389, USA
Tom P. Robertson - Department of Physiology and Pharmacology, Institute of Comparative Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389, USA
James N. Bates - University of Iowa, Anesthesia
Resource Type: Journal article
Publication Details: Vascular pharmacology, Vol.44(6), pp.476-490
Publisher: Elsevier Inc
DOI: 10.1016/j.vph.2006.03.013
PMID: 16697269
ISSN: 1537-1891
eISSN: 1879-3649
Language: English
Date published: 06/01/2006
Academic Unit: Anesthesia
Record Identifier: 9984424843602771

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