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Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
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 wk. PO2
reduction to 40-45 mmHg, the stable prostacyclin analog iloprost
(10 pg/ml), and stimulatory G 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 a LS
diet. Arteries from rats on a 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
1 · min1
iv) restored normal responses to reduced PO2
and iloprost in arteries from animals on a HS diet. These observations
suggest that angiotensin II suppression with a HS diet leads to
impaired relaxation of cerebral arteries in response to vasodilator
stimuli acting at the cell membrane.
salt intake; hypertension; angiotensin; hypoxia; vascular smooth muscle; endothelium
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