Light-activated release of nitric oxide from vascular smooth muscle of normotensive and hypertensive rats.

A porphyrinic sensor was used to monitor nitric oxide release from vascular smooth muscle in response to exposure to ultraviolet light. Aortic rings exposed to UV light relaxed with a time course that parallels this observed NO release. With repeated UV light treatments, the magnitude of the relaxations diminished, suggesting that a store of NO was being exhausted. Photorelaxation in response to UV light was studied in aortic ring from two types of hypertensive rats, genetic (SHRSP) and nitroarginine-induced. These aortic rings showed greater photorelaxation and evidenced less tolerance than did aortic rings from control normotensive rats. Since NO synthase activity is depressed in both types of hypertension, it appears, paradoxically, that the UV light-releasable store of NO is augmented when NO synthase activity is depressed.