Effect of estrogen on flow-induced dilation in NO deficiency: role of prostaglandins and EDHF

被引:51
作者
Huang, A [1 ]
Wu, YM [1 ]
Sun, D [1 ]
Koller, A [1 ]
Kaley, G [1 ]
机构
[1] New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA
关键词
ovariectomy; estrogen replacement; potassium channels; arterioles; endothelium-derived hyperpolarizing factor; nitric oxide;
D O I
10.1152/jappl.2001.91.6.2561
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
To investigate the role of estrogen in flow-induced dilation (FiD) in nitric oxide (NO) deficiency, FiD was examined in isolated gracilis arterioles of ovariectomized (OVX) and OVX rats with estrogen replacement (OVE). Both groups of rats were treated chronically with N-omega-nitro-L-arginine methyl ester. Plasma concentration of NO2/NO3 was reduced in both groups. Plasma concentration of estradiol was lower in OVX than in OVE rats. FiD was similar in vessels of the two groups; calculated wall shear stress and basal tone were significantly greater in OVX vs. OVE rats. Indomethacin did not affect FiD in vessels from OVE, rats but abolished dilation in vessels from OVX rats. Valeryl salicylate or NS-398 inhibited FiD by similar to 50%, whereas their simultaneous administration eliminated the response in arterioles from OVX rats. In vessels from OVE rats, miconazole or charybdotoxin eliminated FiD. Thus, in NO deficiency, prostaglandins derived from both cyclooxygenase isoforms mediate FiD in gracilis arterioles of OVX rats. Estrogen replacement switches the mediation, showing dependence on endothelium-derived hyperpolarizing factor in the arterioles of OVE rats.
引用
收藏
页码:2561 / 2566
页数:6
相关论文
共 31 条
[21]   Role of sex differences and effects of endothelial NO synthase deficiency in responses of carotid arteries to serotonin [J].
Lamping, KG ;
Faraci, FM .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (04) :523-528
[22]   Sex differences in the relative contributions of nitric oxide and EDHF to agonist-stimulated endothelium-dependent relaxations in the rat isolated mesenteric arterial bed [J].
McCulloch, AI ;
Randall, MD .
BRITISH JOURNAL OF PHARMACOLOGY, 1998, 123 (08) :1700-1706
[23]  
Miura H, 2001, CIRCULATION, V103, P1992
[24]  
Morisset S, 1998, J RHEUMATOL, V25, P1146
[25]   Roles of NO and Ca2+-activated K+ channels in coronary vasodilation induced by 17 beta-estradiol in ischemic heart failure [J].
Node, K ;
Kitakaze, M ;
Kosaka, H ;
Minamino, T ;
Sato, H ;
Kuzuya, T ;
Hori, M .
FASEB JOURNAL, 1997, 11 (10) :793-799
[26]   Upregulation of prostacyclin synthesis-related gene expression by shear stress in vascular endothelial cells [J].
Okahara, K ;
Sun, B ;
Kambayashi, J .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (12) :1922-1926
[27]   NITRIC-OXIDE ACTIVATES CYCLOOXYGENASE ENZYMES [J].
SALVEMINI, D ;
MISKO, TP ;
MASFERRER, JL ;
SEIBERT, K ;
CURRIE, MG ;
NEEDLEMAN, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (15) :7240-7244
[28]   Enhanced release of prostaglandins contributes to flow-induced arteriolar dilation in eNOS knockout mice [J].
Sun, D ;
Huang, A ;
Smith, CJ ;
Stackpole, CJ ;
Connetta, JA ;
Shesely, EG ;
Koller, A ;
Kaley, G .
CIRCULATION RESEARCH, 1999, 85 (03) :288-293
[29]   Role of endothelial [Ca2+]i in activation of eNOS in pressurized arterioles by agonists and wall shear stress [J].
Ungvari, Z ;
Sun, D ;
Huang, A ;
Kaley, G ;
Koller, A .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 281 (02) :H606-H612
[30]  
White RM, 2000, J PHARMACOL EXP THER, V292, P375