PHOTOACTIVABLE SOURCE OF RELAXING FACTOR IN GENETIC-HYPERTENSION

Deendothelialized rings of rabbit aorta relax after exposure to UV lig ht because of release of a relaxing factor that is similar if not iden tical to nitric oxide. We tested the hypothesis that production of the photo-induced relaxing factor is impaired in a rat model of genetic h ypertension. Thoracic aortas were removed from adult Wistar-Kyoto rats and stroke-prone spontaneously hypertensive rats. The vessels were cu t into rings, denuded of endothelium, and placed in a muscle bath for isometric force measurement. Rings were contracted with phenylephrine, and relaxation was measured after exposure to UV light. Aortic rings from stroke-prone spontaneously hypertensive rats relaxed to a greater extent after exposure to UV light than did rings from Wistar-Kyoto ra ts. An inhibitor of nitric oxide synthase (N-omega-nitro-L-arginine) g reatly potentiated the relaxation responses to light in both strains, and these enhanced relaxations were attenuated by tetraethylammonium c hloride, potassium chloride, ouabain, or inhibitors of guanylate cycla se. These results suggest that UV irradiation induces relaxation in ao rtic smooth muscle that is greater in hypertensive than normotensive r ats and is greatly enhanced after addition of inhibitors of nitric oxi de production. Thus, the unidentified photo-induced relaxing factor is not solely nitric oxide but may also represent either a hyperpolarizi ng factor, because depolarization blocks the responses entirely, or po ssibly smooth muscle guanylate cyclase that might itself be photoactiv able.