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Cui Hong

First Clinical Institute，China Medical University. Shenyang 110001,Liaoning, China

Abstract

The signal transduction pathways of the inhibitory effect of nitric oxide (NO) on endothelin (ET)-induced proliferation of vascular smooth muscle cells (VSMCs) were studied.3H-thymidine(TdR) incorporation, mitogen-activated protein kinase (MAPK)activity and protein kinase C (PKC) activity of cultured VSMCs of rabbits thoracic aorta were measured in the presence of either NO precursor L-arginine (L-Arg) or NO donor 3 morpholino sydnonimine-hydrochloride (SIN-1), or ET-1 alone or with L-Arg or SIN-1.The results show: (1) ET-1 (10-8 mol/L) significantly increased VSMCs 3H-TdR incorporation (5 times, P <0.01), MAPK activity (4 times, P < 0.01) and PKC activity (3 times, P <0.01 ), as compared with control. L-Arg or SIN-1 alone was without effect on 3H-TdR incorporation, MAPK activity and PKC activity. (2) When ET1 and L-Arg (2, 5, 10 mmol/L) were simultaneously administered, 3H-TdR incorporation and activity of both MAPK and PKC were all significantly dacreased in comparison with the ET group.

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Citing This Article：

Cui Hong. . Acta Physiol Sin 1998; 50 (4): (in Chinese with English abstract).