Abstract
Differences in the influences of endothelium-derived nitric oxside (NO) on α-agonistsinduced contraction in the aortae of spontaneously hypertensive and normotensive rats were studied by blocking NO synthesis with NG-nitro-L-arginine (L-NNA). L-NNA potentiated the contraction induced by noradrenaline. The potentiation was smaller in the preparation from stroke-prone spontaneously hypertensive rats (SHRSP) than in the preparation from Wistar Kyoto rats (WKY). Similar potentiation was observed in the contraction induced by phenylephrine; the potentiation was also smaller in the preparation from SHRSP. α2-agonists, clonidine and UK-14304 induced dose-dependent contraction only in the presence of L-NNA. The dose-response curves for α2-agonists in SHRSP aorta were different from those in WKY aorta; the maximum tension was observed at the concentration of 10-6 M in the preparation from WKY, while the contraction further increased up to 10-4 M in the preparation from WKY. Noradrenaline, clonidine and UK-14304 but not phenyrephrine induced relaxation which was blocked by L-NNA. The relaxation was impaired in the preparation from SHRSP in greater extent than that by acetylcholine. It is suggested that basic or noradrenaline-stimulated NO release from endothelium decreased in the preparation from SHRSP and that α2-adrenoceptor of both the endothelium and smooth muscle may be altered in the preparation from SHRSP.
