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This Article Full Text Full Text (PDF) All Versions of this Article: 582/3/1349    most recent jphysiol.2007.132563v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Coney, A. M. Articles by Marshall, J. M. Search for Related Content PubMed PubMed Citation Articles by Coney, A. M. Articles by Marshall, J. M. Related Collections Integrative

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

There is evidence that sympathetically evoked vasoconstriction in skeletal muscle is blunted in systemic hypoxia, but the mechanisms underlying this phenomenon are not clear. In Saffan-anaesthetized Wistar rats, we have studied the role of ₂-adrenoceptors and neuropeptide Y (NPY) Y₁ receptors in mediating vasoconstriction evoked by direct stimulation of the lumbar sympathetic chain by different patterns of impulses in normoxia (N) and systemic hypoxia (H: breathing 8% O₂). Patterns comprised 120 impulses delivered in bursts over a 1 min period at 40 or 20 Hz, or continuously at 2 Hz. Hypoxia attenuated the evoked increases in femoral vascular resistance (FVR) by all patterns, the response to 2 Hz being most affected (40 Hz bursts: N = 3.25 ± 0.75 arbitrary resistance units (RU); H = 1.14 ± 0.29 RU). Yohimbine (Yoh, ₂-adrenoceptor antagonist) or BIBP 3226 (Y₁-receptor antagonist) did not affect baseline FVR. In normoxia, Yoh attenuated the responses evoked by high frequency bursts and 2 Hz, whereas BIBP 3226 only attenuated the response to 40 Hz (40 Hz bursts: N + Yoh = 2.1 ± 0.59 RU; N + BIBP 3226 = 1.9 ± 0.4 RU). In hypoxia, Yoh did not further attenuate the evoked responses, but BIBP 3226 further attenuated the response to 40 Hz bursts. These results indicate that neither ₂-adrenoceptors nor Y₁ receptors contribute to basal vascular tone in skeletal muscle, but both contribute to constrictor responses evoked by high frequency bursts of sympathetic activity. We propose that in systemic hypoxia, the ₂-mediated component represents about 50% of the sympathetically evoked constriction that is blunted, whereas the contribution made by Y₁ receptors is resistant. Thus we suggest the importance of NPY in the regulation of FVR and blood pressure increases during challenges such as systemic hypoxia.

(Received 20 March 2007; accepted after revision 14 May 2007; first published online 17 May 2007)
Corresponding author A. M. Coney: Department of Physiology, The Medical School, Birmingham B15 2TT, UK. Email: a.m.coney{at}bham.ac.uk

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