Hindlimb unweighting does not alter vasoconstrictor responsiveness and nitric oxide-mediated inhibition of sympathetic vasoconstriction

We tested the hypothesis that physical inactivity would increase sympathetic vasoconstrictor responsiveness and diminish NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague-Dawley rats (n = 33) were randomly assigned to sedentary time control (S) or hindlimb unweighted (HU) groups for 21 days. Following the intervention, rats were anaesthetized and instrumented for measurement of arterial blood pressure and femoral artery blood flow and stimulation of the lumbar sympathetic chain. 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 before (control) and after NO synthase blockade with L-NAME (5 mg kg I.V.). Sympathetic vasoconstrictor responsiveness was not different (P > 0.05) in S and HU rats at rest (S, 2 Hz,-26 +/- 8% and 5 Hz, -46 +/- 12%; and HU, 2 Hz, -29 +/- 9% and 5 Hz, -51 +/- 10%) and during contraction (S, 2 Hz,-10 +/- 7% and 5 Hz,-23 +/- 11%; andHU, 2 Hz,-9 +/- 5% and 5 Hz,-22 +/- 7%). Nitric oxide synthase blockade caused a similar increase (P > 0.05) in sympathetic vasoconstrictor responsiveness in HU and S rats at rest (S, 2 Hz, -41 +/- 7% and 5 Hz, -58 +/- 8%; and HU, 2 Hz, -43 +/- 6% and 5 Hz, -63 +/- 8%) and during muscle contraction (S, 2 Hz, -15 +/- 6% and 5 Hz, -31 +/- 11%; and HU, 2 Hz, -12 +/- 5% and 5 Hz, -29 +/- 8%). Skeletal muscle NO synthase expression and ACh-mediated vasodilatation were also not different between HU and S rats. These data suggest that HU does not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.