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Articles in PresS, published online ahead of print November 27, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00835.2002
Submitted on September 18, 2002
Accepted on November 25, 2002
1 Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
* To whom correspondence should be addressed. E-mail: jlombard{at}mcw.edu.
Male Sprague Dawley rats were maintained on a low salt (LS) diet (0.4 % NaCl) or a (high salt) HS diet (4% NaCl) for 3 days or 4 weeks. PO2 reduction to 40-45 mmHg, the stable prostacyclin analogue iloprost (10 pg/ml), and Gs protein activation with cholera toxin (1 ng/ml) caused vascular smooth muscle (VSM) hyperpolarization, increased cAMP production, and dilation in cerebral arteries from rats on LS diet. Arteries from rats on HS diet exhibited VSM depolarization and constriction in response to hypoxia and iloprost, failed to dilate or hyperpolarize in response to cholera toxin, and cAMP production did not increase in response to hypoxia, iloprost, or cholera toxin. Low dose angiotensin II infusion (5 ng/kg/min, i.v.) restored normal responses to reduced PO2 and iloprost in arteries from animals on a HS diet. These observations suggest that angiotensin II suppression with HS diet leads to impaired relaxation of cerebral arteries in response to vasodilator stimuli acting at the cell membrane.
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