Repriming of Vascular Smooth Muscle Photorelaxation is Dependent upon Endothelium-derived Nitric Oxide

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Abstract
Precontracted vascular smooth muscle (VSM) relaxes when irradiated with visible or UV light. Recent evidence indicates that VSM cells contain a finite store of a photosensitive precursor which is capable of releasing nitric oxide (NO) on exposure to light. Here we report that the store can be exhausted rapidly, by irradiating vessels with laser light. Regeneration of the store occurs spontaneously in the dark. The repriming process displays an absolute requirement for endothelium-derived NO. It is impaired by mechanical damage to the endothelium, and also by treatment of intact vessels with either NG monomethyl-L-arginine or oxyhaemoglobin. Pretreating vessels with ethacrynic acid, a thiol alkylating agent, also prevents repriming of the store. Conversely, bolus injections of authentic NO or S-nitroso-N-acetyl penicillamine accelerate repriming in intact vessels and restore photorelaxation in endothelium-deficient preparations. We conclude that photorelaxation is caused by the release of NO from a photosensitive nitrosothiol(s), generated within VSM cells from tissue-bound thiols and endothelium-derived NO.

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