ENDOTHELIUM-DEPENDENT VASORELAXATION EVOKED BY DESMOPRESSIN AND INVOLVEMENT OF NITRIC-OXIDE IN RAT AORTA

被引:33
作者
YAMADA, K [1 ]
NAKAYAMA, M [1 ]
NAKANO, H [1 ]
MIMURA, N [1 ]
YOSHIDA, S [1 ]
机构
[1] CHIBA UNIV,SCH MED,CHIBA 260,JAPAN
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 264卷 / 02期
关键词
NITRIC OXIDE PRODUCTION;
D O I
10.1152/ajpendo.1993.264.2.E203
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
It is known that in vivo administration of desmopressin (DDAVP; a selective V2-vasopressin receptor agonist) results in prostacyclin-independent vasodilation. The in vitro effects of DDAVP and its mechanisms were examined using rat aortic strips. DDAVP from a concentration of 1 x 10(-9) M caused a concentration-dependent relaxation of the aorta precontracted with norepinephrine (10(-7) M) with intact endothelium. However, no relaxation was induced in aorta with the endothelium removed. The DDAVP-induced relaxation was not influenced by the presence of indomethacin but was inhibited by L-N(G)-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide (NO) synthesis. The inhibition by L-NMMA was reversed by the addition of L-arginine but not D-arginine. Further, the endothelium-dependent relaxation due to DDAVP was potentiated by superoxide dismutase, a scavenger of superoxide anions, and was inhibited by hemoglobin. DDAVP induced an increase in guanosine 3', 5'-cyclic monophosphate levels in the aorta with endothelium but not in aorta without endothelium, and this was suppressed by L-NMMA and hemoglobin. The suppression by L-NMMA was also partially reversed by L-arginine but not by D-arginine. Two selective V2-receptor antagonists had no effect on the DDAVP-induced vasorelaxation. Selective V1-receptor antagonists (a peptidic and a nonpeptidic) caused a concentration-dependent but nonparallel shift to the right of the concentration-response curves to DDAVP. However, DDAVP did not affect the tension of the strip with or without endothelium in nonprecontracted aorta. This evidence suggests that DDAVP evokes the endothelium-dependent in vitro vasorelaxation that is caused by DDAVP-induced NO production in the endothelium. This action is not via the authentic V2 receptor but rather via the endothelial V1-like receptors, which are functionally different from the V1 receptor in smooth muscle cells.
引用
收藏
页码:E203 / E207
页数:5
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