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Salt-induced ANG II suppression impairs the response of cerebral artery smooth muscle cells to prostacyclin

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin

Submitted 5 August 2004 ; accepted in final form 11 October 2004

Recent studies have demonstrated that cerebral arteries from rats fed a high-salt (HS) diet exhibit impaired vasodilation and altered electrophysiological response to reduction in PO₂. The present study examined whether an increase in salt intake alters the response of vascular smooth muscle cells (VSMC) to prostacyclin, a crucial mediator of hypoxic dilation in cerebral arteries. VSMC were isolated from cerebral arteries of male Sprague-Dawley rats maintained on an HS (4% NaCl) or a low-salt diet (0.4% NaCl) for 3 days. The stable prostacyclin analog iloprost (10 ng/ml) inhibited serotonin (0.1–10 µM)-induced contractions and the increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) in VSMC isolated from arteries of animals fed the low-salt diet. In contrast, iloprost had no effect on serotonin-induced contractions and increases in [Ca²⁺]_i in VSMC isolated from arteries of rats fed the HS diet. Preventing the fall in ANG in rats fed the HS diet by infusion of a low dose of ANG II (5 ng·kg^–1·min^–1 iv) restored the inhibitory effect of iloprost on serotonin-induced contractions and increases in [Ca²⁺]_i in VSMC from animals fed the HS diet. These effects were reversed by AT₁ receptor blockade with losartan. These results indicate that ANG II suppression secondary to elevated dietary salt intake impairs vascular relaxation and Ca²⁺ regulation by prostacyclin.

salt intake; hypertension; angiotensin; vascular smooth muscle; calcium; serotonin

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