Hindlimb unweighting does not alter vasoconstrictor responsiveness and XXXX -mediated inhibition of sympathetic vasoconstriction.

@entity842 @entity3451 @entity35 @entity6462 @entity65
KEY POINTS: Physical inactivity increases the risk of @entity65 and may alter sympathetic nervous system control of vascular resistance. Hindlimb unweighting (HU), a rodent model of physical inactivity, has been shown to diminish sympathetic vasoconstrictor responsiveness and reduce NO synthase expression in isolated skeletal muscle blood vessels. Our understanding of the effects of HU on sympathetic vascular regulation in vivo is very limited. The present findings demonstrate that HU did not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. This study suggests that short-term physical inactivity does not alter in vivo sympathetic vascular control in the skeletal muscle vascular bed at rest and during contraction. ABSTRACT: 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. @entity35 (n  =  33) were randomly assigned to sedentary time control (S) or hindlimb unweighted (HU) groups for 21  days. Following the intervention, @entity35 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 @entity6462 (5  mg  kg  i.v.). Sympathetic vasoconstrictor responsiveness was not different (P  >  0.05) in S and HU @entity35 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%; and HU, 2  Hz, -9      5% and 5  Hz, -22      7%). @entity842 synthase blockade caused a similar increase (P  >  0.05) in sympathetic vasoconstrictor responsiveness in HU and S @entity35 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 @entity3451 -mediated vasodilatation were also not different between HU and S @entity35 . These data suggest that HU does not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.
