Estrogen reduces mouse cerebral artery tone through endothelial NOS- and cyclooxygenase-dependent mechanisms

被引:131
作者
Geary, GG [1 ]
Krause, DN [1 ]
Duckles, SP [1 ]
机构
[1] Univ Calif Irvine, Coll Med, Dept Pharmacol, Irvine, CA 92697 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2000年 / 279卷 / 02期
关键词
cerebral arteries; gender; nitric oxide synthase;
D O I
10.1152/ajpheart.2000.279.2.H511
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Gender and estrogen status are known to influence the incidence and severity of cerebrovascular disease. The vasoprotective effects of estrogen are thought to include both nitric oxide-dependent and independent mechanisms. Therefore, using small, resistance-sized arteries pressurized in vitro, the present study determined the effect of gender and estrogen status on myogenic reactivity of mouse cerebral arteries. Luminal diameter was measured in middle cerebral artery segments from males and from females that were either untreated, ovariectomized (OVX), or OVX with estrogen replacement (OVX + EST). The maximal passive diameters of arteries from all four groups were similar. In response to increases in transmural pressure, diameters of arteries from males and OVX females were smaller compared with diameters of arteries from either untreated or OVX + EST females. In the presence of N-G-nitro-L-arginine methyl ester, artery diameters decreased in all groups, but diameters remained significantly smaller in arteries from males and OVX females compared with untreated and OVX + EST females. After endothelium removal or when inhibition of nitric oxide synthase and cyclooxygenase were combined, differences in diameters of arteries from OVX and OVX + EST were abolished. These data suggest that chronic estrogen treatment modulates myogenic reactivity of mouse cerebral arteries through both endothelium-derived cyclooxygenase- and nitric oxide synthase-dependent mechanisms.
引用
收藏
页码:H511 / H519
页数:9
相关论文
共 55 条
[1]   Gender-linked brain injury in experimental stroke [J].
Alkayed, NJ ;
Harukuni, I ;
Kimes, AS ;
London, ED ;
Traystman, RJ ;
Hurn, PD .
STROKE, 1998, 29 (01) :159-165
[2]   ESTROGEN AND CORONARY HEART-DISEASE IN WOMEN [J].
BARRETTCONNOR, E ;
BUSH, TL .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1991, 265 (14) :1861-1867
[3]  
Bayliss WM, 1902, J PHYSIOL-LONDON, V28, P220
[4]   ESTROGEN PRETREATMENT DIRECTLY POTENTIATES ENDOTHELIUM-DEPENDENT VASORELAXATION OF PORCINE CORONARY-ARTERIES [J].
BELL, DR ;
RENSBERGER, HJ ;
KORITNIK, DR ;
KOSHY, A .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1995, 268 (01) :H377-H383
[5]   Estrogen reduces proliferation and agonist-induced calcium increase in coronary artery smooth muscle cells [J].
Bhalla, RC ;
Toth, KF ;
Bhatty, RA ;
Thompson, LP ;
Sharma, RV .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 272 (04) :H1996-H2003
[6]  
Case J, 1999, J PHARMACOL EXP THER, V291, P524
[7]  
CaulinGlaser T, 1997, CIRC RES, V81, P885
[8]   Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice [J].
Chataigneau, T ;
Félétou, M ;
Huang, PL ;
Fishman, MC ;
Duhault, J ;
Vanhoutte, PM .
BRITISH JOURNAL OF PHARMACOLOGY, 1999, 126 (01) :219-226
[9]   Estrogen reduces myointimal proliferation after balloon injury of rat carotid artery [J].
Chen, SJ ;
Li, HB ;
Durand, J ;
Oparil, S ;
Chen, YF .
CIRCULATION, 1996, 93 (03) :577-584
[10]   TRANSDUCTION MECHANISMS INVOLVED IN THE REGULATION OF MYOGENIC ACTIVITY [J].
DANGELO, G ;
MEININGER, GA .
HYPERTENSION, 1994, 23 (06) :1096-1105