Βeta-adrenergic receptors and opposition of evoked sympathetic vasoconstriction: Effects of sex and exercise training

  • Author / Creator
    Cooper, Ian R
  • Stimulation of the sympathetic nervous system evokes the release of neurotransmitters and produces vasoconstriction that is primarily mediated by the binding of norepinephrine (NE) to alpha-adrenergic receptors. However, NE may also bind to beta (β)-adrenergic receptors and produce vasodilation that may oppose vasoconstriction. Exercise training has been shown to enhance contraction-mediated inhibition of sympathetic vasoconstriction (sympatholysis), however the underlying mechanism(s) have not been fully established. It is possible that exercise training may up-regulate β- adrenergic receptor mediated vasodilation and blunt vasoconstrictor responses. Furthermore, β-adrenergic receptor function in the peripheral vasculature may be sex- specific with beta-receptor mediated vasodilation being more important in the regulation of peripheral vascular resistance in females compared to males. Therefore the present study sought to determine if β-adrenergic receptor mediated vasodilation inhibits sympathetic vasoconstrictor responses in resting and contracting skeletal muscle. Additionally the present study investigated the effects of exercise training and sex on β- adrenergic receptor mediated opposition of evoked sympathetic vasoconstriction. It was hypothesized that β-adrenergic receptors would oppose evoked sympathetic vasoconstriction at rest and during exercise in females, but would not oppose sympathetic vasoconstriction in males. Additionally it was hypothesized that exercise training would augment β-adrenergic receptor mediated opposition to evoked sympathetic vasoconstriction in females. Male (n=18) and Female (n=17) Sprague-Dawley rats were randomized into Sedentary (S) or Exercise Trained (ET) groups. ET rats completed a 4- week treadmill training regimen (5 days/week, 15 min at 40m/min). At the completion of 2 ET or S, rats were anaesthetized and instrumented for the measurement of femoral vascular conductance (FVC), stimulation of the lumbar sympathetic chain, and contraction of the triceps surae muscle group. The percentage change of femoral vascular conductance (FVC) in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction (60% maximal contractile force) before (Control) and after β-adrenergic blockade (propranolol; 0.075mg/kg body mass, I.V.). Contrary to the hypothesis, β-adrenergic blockade decreased evoked sympathetic vasoconstriction (P < 0.05), and was not different between males and females at rest (P > 0.05). During skeletal muscle contraction, female rats had lower responses to evoked sympathetic vasoconstriction than males (P < 0.05), but it was not altered by β-adrenergic blockade (P > 0.05). In contrast to previous research from our laboratory, exercise training did not alter (P > 0.05) sympathetic vasoconstrictor responsiveness or inhibition of sympathetic vasoconstriction. The present study demonstrates that β-adrenergic receptors do not oppose sympathetic vasoconstriction at rest or during skeletal muscle contraction in the hindlimb of rats and at rest are not different between males and females. However during skeletal muscle contraction, females demonstrate a greater attenuation of evoked sympathetic vasoconstriction that was not altered by β-adrenergic receptor antagonism. Collectively, the results from this study suggest that β-adrenergic receptors do not oppose evoked vasoconstrictor responses in resting and contracting skeletal muscle. This study also demonstrated that contraction-mediated inhibition of sympathetic vasoconstriction is greater in female compared to rats. The enhanced blunting of vasoconstriction in female rats was not altered by exercise training and does not appear to be mediated by β-adrenergic receptors.

  • Subjects / Keywords
  • Graduation date
    Fall 2016
  • Type of Item
  • Degree
    Master of Science
  • DOI
  • License
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