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The Journal of physiology

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


PMID 25752721

Abstract

Physical inactivity increases the risk of cardiovascular disease 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. 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 (nxa0=xa033) were randomly assigned to sedentary time control (S) or hindlimb unweighted (HU) groups for 21xa0days. 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 5xa0Hz was determined at rest and during triceps surae muscle contraction before (control) and after NO synthase blockade with l-NAME (5xa0mgxa0kgxa0i.v.). Sympathetic vasoconstrictor responsiveness was not different (Pxa0>xa00.05) in S and HU rats at rest (S, 2xa0Hz, -26xa0±xa08% and 5xa0Hz, -46xa0±xa012%; and HU, 2xa0Hz, -29xa0±xa09% and 5xa0Hz, -51xa0±xa010%) and during contraction (S, 2xa0Hz, -10xa0±xa07% and 5xa0Hz, -23xa0±xa011%; and HU, 2xa0Hz, -9xa0±xa05% and 5xa0Hz, -22xa0±xa07%). Nitric oxide synthase blockade caused a similar increase (Pxa0>xa00.05) in sympathetic vasoconstrictor responsiveness in HU and S rats at rest (S, 2xa0Hz, -41xa0±xa07% and 5xa0Hz, -58xa0±xa08%; and HU, 2xa0Hz, -43xa0±xa06% and 5xa0Hz, -63xa0±xa08%) and during muscle contraction (S, 2xa0Hz, -15xa0±xa06% and 5xa0Hz, -31xa0±xa011%; and HU, 2xa0Hz, -12xa0±xa05% and 5xa0Hz, -29xa0±xa08%). 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.

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