Alteration in the release of endothelium-derived relaxing factors by alpha-adrenoceptor stimulation in the aorta of stroke-prone spontaneously hypertensive rats.

1. Endothelium-dependent relaxation by alpha-adrenoceptor agonists was examined in the thoracic aorta from normotensive Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP). 2. In ring preparations from both strains, noradrenaline-induced contraction was increased by L-nitro arginine (L-NNA), a NO synthesis inhibitor. 3. L-NNA increased the contraction induced by phenylephrine, an alpha1-adrenoceptor agonist. UK-14304 and clonidine, alpha2-adrenoceptor agonists, did not contract the preparations with intact endothelium. However, these agents contracted preparations when NO synthesis was inhibited. 4. In a precontracted preparation, clonidine and UK-14304 induced relaxations. The relaxations in SHRSP aorta were smaller than those in WKY aorta. 5. These results indicate that alpha-agonists release NO from endothelium in WKY and SHRSP aorta. The mechanism related to NO release by alpha2-adrenoceptor agonist is impaired in SHRSP aorta.