Nitric oxide modulation of coronary artery myogenic tone in spontaneously hypertensive and Wistar-Kyoto rats

被引:18
作者
Garcia, SR [1 ]
Bund, SJ [1 ]
机构
[1] Univ Manchester, Manchester Royal Infirm, Dept Med, Manchester M13 9WL, England
关键词
coronary artery; cyclooxygenase; endothelium; hypertension; indomethacin; myogenic tone; N-omega-nitro-L-arginine; nitric oxide; spontaneously hypertensive rat;
D O I
10.1042/cs0940225
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
1, The endothelium contributes substantially to the modulation of myogenic tone in coronary arteries from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), This study has addressed the contributions of endothelium-derived nitric oxide and cyclo-oxygenase products to this modulation in small coronary arteries (approximately 200 mu m internal diameter) from 20-week-old SHR and WKY under pressurized, no-flow conditions in an arteriograph. 2, Active pressure-diameter relationships were uninfluenced by the cyclo-oxygenase inhibitor indomethacin (10 mu mol/l) in either rat strain, In the presence of indomethacin and the nitric oxide synthase inhibitor N-omega-nitro-L-arginine (L-NNA, 0.1 mmol/l), coronary arteries from SHR and WKY generated significantly greater myogenic tone, This increase in tone was similar in both strains, 3, In endothelium-denuded arteries, indomethacin and L-NNA did not influence tone, 4, Therefore, these results demonstrate that endothelium-derived nitric oxide is basally released to attenuate SHR and WKY coronary artery myogenic tone, whereas endothelium-derived cyclo-oxygenase products have no net vasoactive influence, Additionally, these data suggest that basal nitric oxide-mediated relaxation is normal in SHR coronary arteries and is therefore unlikely to be a pathogenic mechanism in this animal model of hypertension.
引用
收藏
页码:225 / 229
页数:5
相关论文
共 40 条
[1]   Reciprocal inhibition of nitric oxide and prostacyclin synthesis in human saphenous vein [J].
Barker, JE ;
Bakhle, YS ;
Anderson, J ;
Treasure, T ;
Piper, PJ .
BRITISH JOURNAL OF PHARMACOLOGY, 1996, 118 (03) :643-648
[2]   Nitric oxide attenuates the release of endothelium-derived hyperpolarizing factor [J].
Bauersachs, J ;
Popp, R ;
Hecker, M ;
Sauer, E ;
Fleming, I ;
Busse, R .
CIRCULATION, 1996, 94 (12) :3341-3347
[3]   ENDOTHELIUM-DEPENDENT MODULATION OF RESISTANCE VESSEL CONTRACTION - STUDIES WITH NG-NITRO-L-ARGININE METHYL-ESTER AND NG-NITRO-L-ARGININE [J].
BENNETT, MA ;
WATT, PAC ;
THURSTON, H .
BRITISH JOURNAL OF PHARMACOLOGY, 1992, 107 (02) :616-621
[4]   IMPORTANCE OF BASAL NITRIC-OXIDE SYNTHESIS IN REGULATION OF MYOCARDIAL BLOOD-FLOW [J].
BENYO, Z ;
KISS, G ;
SZABO, C ;
CSAKI, C ;
KOVACH, AGB .
CARDIOVASCULAR RESEARCH, 1991, 25 (08) :700-703
[5]   NITRIC-OXIDE IS AN IMPORTANT DETERMINANT OF CORONARY FLOW IN THE ISOLATED BLOOD PERFUSED RAT-HEART [J].
BOUMA, P ;
FERDINANDY, P ;
SIPKEMA, P ;
ALLAART, CP ;
WESTERHOF, N .
BASIC RESEARCH IN CARDIOLOGY, 1992, 87 (06) :570-584
[6]  
COHEN RA, 1988, J PHARMACOL EXP THER, V244, P550
[7]   ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION - BEYOND NITRIC-OXIDE AND CYCLIC-GMP [J].
COHEN, RA ;
VANHOUTTE, PM .
CIRCULATION, 1995, 92 (11) :3337-3349
[8]   Reduced basal NO-mediated dilation and decreased endothelial NO-synthase expression in coronary vessels of spontaneously hypertensive rats [J].
Crabos, M ;
Coste, P ;
Paccalin, M ;
Tariosse, L ;
Daret, D ;
Besse, P ;
BonoronAdele, S .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1997, 29 (01) :55-65
[9]   ENHANCED MYOGENIC ACTIVATION IN SKELETAL-MUSCLE ARTERIOLES FROM SPONTANEOUSLY HYPERTENSIVE RATS [J].
FALCONE, JC ;
GRANGER, HJ ;
MEININGER, GA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (06) :H1847-H1855
[10]   ENDOTHELIAL INDEPENDENCE OF MYOGENIC RESPONSE IN ISOLATED SKELETAL-MUSCLE ARTERIOLES [J].
FALCONE, JC ;
DAVIS, MJ ;
MEININGER, GA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (01) :H130-H135