Release of nitric oxide and prostaglandin H-2 to acetylcholine in skeletal muscle venules

被引:17
作者
Dornyei, G
Kaley, G
Koller, A
机构
[1] NEW YORK MED COLL, DEPT PHYSIOL, VALHALLA, NY 10595 USA
[2] SEMMELWEIS UNIV MED, INST PATHOPHYSIOL, H-1445 BUDAPEST, HUNGARY
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1997年 / 272卷 / 06期
关键词
rat gracilis muscle; venular resistance; endothelium-derived constrictor and dilator factors;
D O I
10.1152/ajpheart.1997.272.6.H2541
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (similar to 225 mu m in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane Az-prostaglandin Hz (PGH(2)) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/-: 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N-omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH(2) from the venular endothelium.
引用
收藏
页码:H2541 / H2546
页数:6
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