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

Nguyen N. P. Tran, Esther Spitzbarth, Alain Robert, Philippe Giummelly, Jeffrey Atkinson and Christine Capdeville-Atkinson *

1. 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).

2. 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-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.

3. Fura-2 loaded into endothelial cells but endothelial 'contamination' of the smooth muscle cell [Ca²⁺]_i signal was minimal.

4. Endogenous NO decreased vasoconstrictor responses to noradrenaline but had no effect on [Ca²⁺]_i.

5. Nitroglycerine decreased vasoconstrictor responses in a concentration-dependent fashion but had no effect on [Ca²⁺]_i.

6. In conclusion, NO causes vasodilatation via a mechanism which is downstream of [Ca²⁺]_i mobilization.

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