J C Frisbee1, J H Lombard. 1. Department of Physiology, Medical College of Wisconsin, Milwaukee 53226, USA. jfrisbee@mcw.edu
Abstract
OBJECTIVE: To determine the development and reversibility of the altered vasodilator reactivity of cremasteric arterioles in rats on high-salt diet and with reduced renal mass hypertension (RRMHT). METHODS: Sprague Dawley rats were fed high-salt (HS) or low-salt (LS) diet and RRMHT rats were fed HS diet (HSRRM) over 4 weeks, after which a group of HS and HSRRM rats were fed LS diet for 4 additional weeks (HS/LS and HS/LSRRM), while all others remained on their original diet. Changes in arteriolar diameter to dilator agonists (acetylcholine, iloprost, cholera toxin, forskolin, and sodium nitroprusside) and to Ca2+ free solution plus adenosine (to determine maximum diameter) were measured with a videomicrometer. RESULTS: Reduced vasodilator reactivity developed over 4 weeks with HS diet and RRMHT, although more rapidly and to a greater extent with RRMHT. In HS rats, the reduced reactivity was completely reversible with restoration of LS diet. Complete recovery of dilator reactivity to control levels did not occur with restoration of LS diet and normotension in HS/LSRRM rats, although the slope of the recovery over the final 4 weeks was comparable to that in normotensive HS/LS animals. CONCLUSIONS: Impaired vasodilator reactivity, occurring with high-salt diet, appears to be fully reversible. Impaired vascular reactivity may recover after restoration of normal blood pressure in RRMHT, although over a longer period than with high-salt diet alone.
OBJECTIVE: To determine the development and reversibility of the altered vasodilator reactivity of cremasteric arterioles in rats on high-salt diet and with reduced renal mass hypertension (RRMHT). METHODS:Sprague Dawley rats were fed high-salt (HS) or low-salt (LS) diet and RRMHT rats were fed HS diet (HSRRM) over 4 weeks, after which a group of HS and HSRRM rats were fed LS diet for 4 additional weeks (HS/LS and HS/LSRRM), while all others remained on their original diet. Changes in arteriolar diameter to dilator agonists (acetylcholine, iloprost, cholera toxin, forskolin, and sodium nitroprusside) and to Ca2+ free solution plus adenosine (to determine maximum diameter) were measured with a videomicrometer. RESULTS: Reduced vasodilator reactivity developed over 4 weeks with HS diet and RRMHT, although more rapidly and to a greater extent with RRMHT. In HSrats, the reduced reactivity was completely reversible with restoration of LS diet. Complete recovery of dilator reactivity to control levels did not occur with restoration of LS diet and normotension in HS/LSRRM rats, although the slope of the recovery over the final 4 weeks was comparable to that in normotensive HS/LS animals. CONCLUSIONS: Impaired vasodilator reactivity, occurring with high-salt diet, appears to be fully reversible. Impaired vascular reactivity may recover after restoration of normal blood pressure in RRMHT, although over a longer period than with high-salt diet alone.
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