The Effect of Beta‐Adrenergic Receptor Blockade on Sympathetic Vasoconstrictor Responsiveness in Sedentary and Exercise‐Trained Female Rats

Abstract

Listen

Translate article

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‐ adrenergic receptors and produce vasodilation that opposes vasoconstriction. Therefore, in the present study, we tested the hypothesis that beta‐adrenergic receptor blockade would augment sympathetic vasoconstrictor responsiveness in resting and contracting skeletal muscle of sedentary and exercise trained female rats, demonstrating beta‐adrenergic receptor mediated opposition of vasoconstriction. We also hypothesized that the increase in sympathetic vasoconstrictor responsiveness in the presence of beta‐adrenergic blockade would be larger in exercise‐trained rats, indicating that exercise training augments beta‐adrenergic receptor mediated opposition of vasoconstriction. Female Sprague‐Dawley rats were randomized to Sedentary (n=8, 265 ± 28 g) and Exercise Trained (n=9, 290 ± 27 g) groups. Exercise Trained rats completed a 4‐week treadmill training regimen (5 d/week, 15 min at 40 m/min, 5% gradient). Subsequently, 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 (Δ%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 beta‐adrenergic blockade (Propranolol; 0.075 mg/kg body mass, I.V.). Sympathetic vasoconstrictor responsiveness (Δ%FVC) was not different (P > 0.05) between Sedentary and Exercise Trained rats at rest or during contraction. At rest, beta‐adrenergic receptor blockade did not increase (P > 0.05) sympathetic vasoconstrictor responsiveness in Sedentary (Control: 2Hz: −34 ± 9 %, 5Hz: −53 ± 8 %; Propranolol: 2Hz: −31 ± 10 %, 5Hz: −49 ± 8 %) or Exercise Trained (Control: 2Hz: −38 ± 9 %, 5Hz: −57 ± 8 %; Propranolol: 2Hz: −34 ± 7 %, 5Hz: −53 ± 8 %) rats. Similarly, beta‐adrenergic receptor blockade did not increase (P > 0.05) sympathetic vasoconstrictor responsiveness during exercise in Sedentary (Control: 2Hz: −7 ± 4 %, 5Hz: −20 ± 11 %; Propranolol: 2Hz: −6 ± 5 %, 5Hz: −18 ± 10 %) or Exercise Trained (Control: 2Hz: −10 ± 8 %, 5Hz: −28 ± 8 %; Propranolol: 2Hz: −6 ± 5 %, 5Hz: −24 ± 12 %) rats. In conclusion, beta‐adrenergic receptor blockade did not augment sympathetic vasoconstrictor responsiveness in resting or contracting skeletal muscle of sedentary or exercise‐trained female rats, suggesting that beta‐adrenergic receptor mediated vasodilation did not oppose vasoconstriction, regardless of training status.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada, Canadian Foundation for Innovation, and Alberta Advanced Education and Technology.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.