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¹ Department of Physiology, The Medical School, Birmingham B15 2TT, UK

Experiments were performed under Saffan anaesthesia on normoxic (N) rats and on chronically hypoxic rats exposed to 12% O₂ for 1, 3 or 7 days (1, 3 or 7CH rats): N rats routinely breathed 21% O₂ and CH rats 12% O₂. The 1, 3 and 7CH rats showed resting hyperventilation relative to N rats, but baseline heart rate (HR) was unchanged and arterial blood pressure (ABP) was lowered. Femoral vascular conductance (FVC) was increased in 1 and 3CH rats, but not 7CH rats. When 1–7CH rats were acutely switched to breathing 21% O₂ for 5 min, ABP increased and FVC decreased, consistent with removal of a hypoxic dilator stimulus that is waning in 7CH rats. We propose that this is because the increase in haematocrit and vascular remodelling in skeletal muscle help restore the O₂ supply. The increases in FVC evoked by acute hypoxia (8% O₂ for 5 min) and by infusion for 5 min of -calcitonin gene-related peptide (-CGRP), which are NO-dependent, were particularly accentuated in 1CH, relative to N rats. The NO synthesis inhibitor L-NAME increased ABP, decreased HR and greatly reduced FVC, and attenuated increases in FVC evoked by acute hypoxia and -CGRP, such that baselines and responses were similar in N and 1–7CH rats. We propose that in the first few days of chronic hypoxia there is tonic NO-dependent vasodilatation in skeletal muscle that is associated with accentuated dilator responsiveness to acute hypoxia and dilator substances that are NO -dependent.

(Received 3 March 2006; accepted after revision 10 May 2006; first published online 11 May 2006)
Corresponding author J. M. Marshall: Department of Physiology, The Medical School, Birmingham B15 2TT, UK. Email: j.m.marshall{at}bham.ac.uk

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