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Chronic AT₁ receptor blockade alters mechanisms mediating responses to hypoxia in rat skeletal muscle resistance arteries

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

Submitted 1 December 2003 ; accepted in final form 15 March 2004

The goal of this study was to determine the effect of angiotensin type 1 (AT₁) receptor antagonism on vasodilator responses in isolated skeletal muscle resistance arteries. Normotensive Sprague-Dawley rats were fed normal rat chow with the AT₁ receptor antagonist losartan (1mg/ml) in the drinking water for 7 days and compared with untreated control rats. Changes in the diameter of isolated resistance arteries supplying the gracilis muscle were assessed with a video micrometer. Arteriolar responses to acetylcholine, iloprost, and sodium nitroprusside were unaffected by losartan administration, whereas dilation to reduced PO₂ was converted into a constriction. Hypoxia-induced constriction of vessels from losartan-treated rats was inhibited by endothelium removal or indomethacin (1 µM). Blockade of the PGH₂-thromboxane A₂ receptor with SQ-29548 (10 µM), thromboxane synthase inhibition with dazoxiben (10 µM), or the addition of the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL, 100 µM) converted hypoxic vasoconstriction to a dilation that was blocked by inhibiting nitric oxide synthase with N-nitro-L-arginine methyl ester (100 µM). These data suggest that AT₁ receptor activation has an important role in maintaining the vascular release of prostaglandins responsible for mediating hypoxic dilation in skeletal muscle microvessels.

angiotensin II; angiotensin II receptors; vascular smooth muscle; endothelium; microcirculation

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