Abstract

This study investigated the hypothesis that β-adrenoreceptor-mediated inhibition of sympathetic vasoconstriction would be enhanced in female compared with male rats, and that endurance exercise training would augment β-adrenoreceptor-mediated inhibition of sympathetic vasoconstriction in male and female rats. Sprague-Dawley rats were randomized into sedentary (male: n = 7; female: n = 8) and exercise-trained (male: n = 9; female: n = 9) groups. Following 4 wk of exercise training or being sedentary, rats were anesthetized and surgically instrumented for stimulation of the lumbar sympathetic chain, muscle contraction and measurement of arterial blood pressure and femoral artery blood flow (FBF). Femoral vascular conductance (FVC) was calculated as FBF/mean arterial pressure. The percentage change of FVC in response to sympathetic stimulation delivered at 2 and 5 Hz was measured at rest and during contraction of the triceps surae muscles before and after β-adrenoreceptor blockade (propranolol: 0.075 mg·kg-1 iv). We found that, at rest, β-adrenoreceptor blockade decreased (main effect of drug, 2 Hz: P < 0.001; 5 Hz: P < 0.001) sympathetic vasoconstriction. During contraction, sympathetic vasoconstrictor responsiveness was lower (main effect of sex, 2 Hz: P = 0.001; 5 Hz: P = 0.023) in female compared with male rats, and sympatholysis was enhanced (main effect of sex, 2 Hz: P = 0.001; 5 Hz: P < 0.001) in female rats. β-adrenoreceptor blockade decreased (main effect of drug, 2 Hz: P = 0.049; 5 Hz: P < 0.001) evoked sympathetic vasoconstriction in contracting muscle. The present study demonstrated that β-adrenoreceptors do not blunt sympathetic vasoconstriction in resting or contracting skeletal muscle of male or female rats. Sympatholysis was enhanced in female rats; however, this was not attributable to β-adrenoreceptor-mediated blunting of sympathetic vasoconstriction.NEW & NOTEWORTHY β-adrenoreceptors do not inhibit sympathetic vasoconstriction in resting or contracting muscle of male or female rats, regardless of training status. Sympatholysis was enhanced in female, compared to male rats; however, β-adrenoreceptors were not responsible for the enhanced sympatholysis. These findings indicate that β-adrenoreceptors do not contribute to the regulation of sympathetic vasoconstriction in resting and contracting skeletal muscle and suggest that β-adrenoreceptors do not underlie sex differences in the neural control of the circulation.

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