Nitric oxide and the mechanism of rat vascular smooth muscle photorelaxation.

Photorelaxation of vascular smooth muscle (VSM) was studied using segments of tail artery from normotensive rats (NTR) or spontaneously hypertensive rats (SHR). Isolated vessels with intact endothelium were perfused with Krebs solution containing phenylephrine. Perfusion pressures were recorded while arteries were irradiated with either visible (VIS; lambda=514.5 nm) or long wavelength ultra-violet (UVA; lambda=366 nm) light. VIS light produced a transient vasodilator response: a rapid decrease of pressure that recovered fully during the period (6 min) of illumination. An irradiated artery was refractory to a second period of illumination delivered immediately after the first, but its photosensitivity recovered slowly in the dark, a process called 'repriming'. Photorelaxations generated by UVA light were qualitatively different and consisted of two components: a phasic (or p-) component superimposed on a sustained (or s-) component. The p-component is similar to the VIS light-induced response in that both exhibit refractoriness and repriming depends upon endothelium-derived NO. In contrast, the s-component persists throughout the period of illumination and does not show refractoriness. We conclude that VIS light-induced photorelaxations and the p-component of UVA light-induced responses are mediated by the photochemical release of NO from a finite molecular 'store' that can be reconstituted afterwards in the dark. The s-component of the UVA light-induced response does not depend directly on endothelial NO and may result instead from a stimulatory effect of UVA light on soluble guanylate cyclase. NO-dependent photorelaxation is impaired in vessels from SHR while the s-component is enhanced.