NOS 만성억제로 인한 고혈압에서 아드레날린성 활성증가기전

Mechanism of Increased Adrenergic Activities in Hyprertension Induced by Chronic Inhibition of NOS

Nitric oxide is a tonically produced vasodilator that maintains blood pressure in the normal animal. The chronic inhibition of nitric synthase (NOS) elicits the hypertension in rats. However, the mechanism of hypertension indused by chronic inhibition of NOS is not clear. Thus, to clarify the mechanism of the occurance of hypretension, the changes in alpha-adrenergic systems in rats treated with NOS inhibitors for 21 days were examined. Chronic administration of L-NAME significantly increased in the basal blood pressure, but chrinic administration of 7-nitroindazole did not. Phenylephrine and G-protein stimulator elicited the more potent contraction in the aorta of the L-NAME-induced hypertensive rats. However when the contractile responses by phenylephrine and G-protein stimulator were calculated the the proportion to the contraction by 24 nM KCL, there was no difference between the vehicle-treated rats and the L-NAME-treated rats. The results suggest that hypertension induced by chronic inhibition of NOS is due to the inhibition of eNOS and the increased reponses to the adrenergic drugs are due to the changes of the intracellular contactile mechanism of aoric tissue rather than the changes of receptor density.