Abstract

We hypothesized that hindlimb unloading (HU) would increase sympathetic vasoconstrictor responsiveness and diminish nitric oxide (NO) mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague‐Dawley rats (n=21) were randomized to sedentary time‐control (S; n = 9) or HU (n = 12) groups for 21d. Rats were anesthetized and instrumented for stimulation of the lumbar sympathetic chain and measurement of femoral vascular conductance (FVC). Sympathetic stimulations were delivered at 2Hz and 5Hz at rest and during contraction of the triceps surae muscles at 60% of maximal contractile force before and after NO synthase blockade (L‐NAME; 5mg·kg‐1 IV). The percentage decrease in FVC in response to sympathetic stimulation was not different (P > 0.05) between groups at rest (HU: 2Hz: ‐29 ± 10%; 5Hz: ‐50 ± 12%; S: 2Hz: ‐26 ± 10%, 5Hz: ‐44 ± 8%) and during contraction (HU: 2Hz: ‐9 ± 4%; 5Hz: ‐22 ± 7%; S: 2Hz: ‐7 ± 5%; 5Hz:‐18 ± 7%). In the presence of L‐NAME the vasoconstrictor response was not different (P > 0.05) between groups at rest (HU: 2Hz: ‐43 ± 7%; 5Hz: ‐63 ± 10%; S: 2Hz: ‐42 ± 8%; 5Hz: ‐57 ± 6%) and during contraction (HU: 2Hz: ‐12 ± 3%; 5Hz: ‐24 ± 6%; S: 2Hz: ‐12 ± 4%; 5Hz: ‐28 ± 8%). We conclude that HU does not alter sympathetic vasoconstrictor responsiveness or NO mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.Grant Funding Source: Supported by NSERC, Canada.

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