Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles.

Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Research Abstract Details 

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Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Abstract Text:

David G Ingram,Sean C Newcomer,Elmer M Price,Kevin E Eklund,Richard M McAllister,M Harold Laughlin,

Current literature suggests that chronic nitric oxide synthase (NOS) inhibition has differential effects on endothelium-dependent dilation (EDD) of conduit arteries vs. arterioles. Therefore, we hypothesized that chronic inhibition of NOS would impair EDD of porcine left anterior descending (LAD) coronary arteries but not coronary arterioles. Thirty-nine female Yucatan miniature swine were included in the study. Animals drank either tap water or water with N(G)-nitro-L-arginine methyl ester (L-NAME; 100 mg/l), resulting in control and chronic NOS inhibition (CNI) groups, respectively. Treatment was continued for 1-3 mo (8.3 +/- 0.6 mg x kg(-1) x day(-1)). In vitro EDD of coronary LADs and arterioles was assessed via responses to ADP (LADs only) and bradykinin (BK), and endothelium-independent function was assessed via responses to sodium nitroprusside (SNP). Chronic NOS inhibition diminished coronary artery EDD to ADP and BK. Incubating LAD rings with L-NAME decreased relaxation responses of LADs from control pigs but not from CNI pigs such that between-group differences were abolished. Neither indomethacin (Indo) nor sulfaphenazole incubation significantly affected relaxation responses of LAD rings to ADP or BK. Coronary arteries from CNI pigs showed enhanced relaxation responses to SNP. In contrast to coronary arteries, coronary arterioles from CNI pigs demonstrated preserved EDD to BK and no increase in dilation responses to SNP. L-NAME, Indo, and L-NAME + Indo incubation did not result in significant between-group differences in arteriole dilation responses to BK. These results suggest that although chronic NOS inhibition diminishes EDD of LAD rings, most likely via a NOS-dependent mechanism, it does not affect EDD of coronary arterioles.

Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Publishing Authors By Initials

DG Ingram,SC Newcomer,EM Price,KE Eklund,RM McAllister,MH Laughlin,

For similar chemical actions and uses: pharmacologic actions: therapeutic uses: cardiovascular agents: vasodilator agents research abstracts see: chemical actions and uses: pharmacologic actions: therapeutic uses: cardiovascular agents: vasodilator agents research

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Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Heart and circulat

VOLUME: 292

Page Numbers: H2798-808

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 26

MONTH: 01

YEAR: 2007

Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Keywords Mesh Terms:

KEYWORDS: Vasodilator Agents

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles. Information

Substance Name: Superoxide Dismutase

Registry Number: EC 1.15.1.1

Grant and Affiliation Information for Chronic nitric oxide synthase inhibition blunts endothelium-dependent function of conduit coronary arteries, not arterioles.

AFFILIATION: Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA.

Country: United States

AGENCY: United States NCRR

GRANT: RR18276

ACRONYM: RR

MEDLINETA: Am J Physiol Heart Circ Physio

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