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Received November 14, 2003
Revised November 28, 2003
Accepted after revision January 6, 2004
1 University of Birmingham
* To whom correspondence should be addressed. E-mail: a.m.coney{at}bham.ac.uk.
We studied the role of nitric oxide (NO) in blunting sympathetically-evoked muscle vasoconstriction during acute and chronic systemic hypoxia. Experiments were performed on anaesthetised normoxic (N) and chronically hypoxic (CH) rats that had been acclimated to 12% O2 for 3-4 weeks. The lumbar sympathetic chain was stimulated for 1min with bursts at 20 or 40Hz and continuously at 2Hz. In N rats, acute hypoxia (breathing 8% O2) reduced baseline femoral vascular resistance (FVR) and depressed increases in FVR evoked by all 3 patterns of stimulation, but infusion of the NO-donor sodium nitroprusside (SNP) so as to similarly reduce baseline FVR, did not affect sympathetically-evoked responses. Blockade of NO synthase (NOS) with L-NAME, increased baseline FVR and facilitated the sympathetically-evoked increases in FVR, but when baseline FVR was restored by SNP infusion, these evoked responses were restored. Acute hypoxia after L-NAME still reduced baseline FVR and depressed evoked responses. In CH rats breathing 12% O2, baseline FVR was lower than in N rats breathing air, but L-NAME had qualitatively similar effects on baseline FVR and sympathetically-evoked increases in FVR. SNP similarly restored baseline FVR and evoked responses. Inhibition of neuronal NOS or inducible NOS did not affect baselines, or evoked responses. We propose that in N and CH rats, sympathetically-evoked muscle vasoconstriction is modulated by tonically-released NO, but not depressed by additional NO released on sympathetic activation. The present results suggest that hypoxia-induced blunting of sympathetic vasoconstriction in skeletal muscle is not mediated by NO.
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