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Nitric Oxide and the Mechanism of Rat Vascular Smooth Muscle Photorelaxation
Author(s) -
Flitney Frederick Werner,
Megson Ian L.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.041970
Subject(s) - phenylephrine , vasodilation , biophysics , vascular smooth muscle , chemistry , nitric oxide , endothelium , blue light , action spectrum , irradiation , perfusion , refractory period , visible spectrum , anatomy , medicine , smooth muscle , biology , blood pressure , optics , physics , organic chemistry , nuclear physics
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; λ= 514.5 nm) or long wavelength ultra‐violet (UVA; λ= 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.