Nitric oxide lowers the calcium sensitivity of tension in the rat tail artery

摘要

class="enumerated" style="list-style-type:decimal">Controversy exists as to whether a fall in the intracellular Ca²⁺ concentration ([Ca²⁺]i) is a requisite element of the vasodilatory response to nitric oxide (NO).We studied the effect of NO on the coupling between [Ca²⁺]i and vasoconstriction in arterial segments loaded with the [Ca²⁺]i-sensitive, intracellular dye fura-2. As data interpretation is equivocal when fura-2 is loaded into both endothelial and smooth muscle cells, we compared results from in vitro experiments on segments of the rat tail artery in which fura-2 and noradrenaline were applied on the luminal or adventitial side, and endothelium was removed ‘physically’ (rubbing or air) or ‘functionally’ (N^ω-nitro-l-arginine methyl ester). The use of air perfusion to remove endothelium is of considerable benefit since it allows paired observations in a single tissue.Fura-2 loaded into endothelial cells but endothelial ‘contamination’ of the smooth muscle cell [Ca²⁺]i signal was minimal.Endogenous NO decreased vasoconstrictor responses to noradrenaline but had no effect on [Ca²⁺]i.Nitroglycerine decreased vasoconstrictor responses in a concentration-dependent fashion but had no effect on [Ca²⁺]i.In conclusion, NO causes vasodilatation via a mechanism which is downstream of [Ca²⁺]i mobilization.