| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Department of Physiology, The Medical School, Birmingham B15 2TT, 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 anaesthetized 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 1 min with bursts at 20 or 40 Hz and continuously at 2 Hz. In N rats, acute hypoxia (breathing 8% O2) reduced baseline femoral vascular resistance (FVR) and depressed increases in FVR evoked by all three 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.
(Received 14 November 2003;
accepted after revision 6 January 2004;
first published online 14 January 2004)
Corresponding author A. M. Coney: Department of Physiology, The Medical School, Birmingham B15 2TT, UK. Email: a.m.coney{at}bham.ac.uk
This article has been cited by other articles:
|
|
 |
|
  A. M. Coney and J. M. Marshall Contribution of {alpha}2-adrenoceptors and Y1 neuropeptide Y receptors to the blunting of sympathetic vasoconstriction induced by systemic hypoxia in the rat J. Physiol., August 1, 2007; 582(3): 1349 - 1359. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. W. Wilkins, W. G. Schrage, Z. Liu, K. C. Hancock, and M. J. Joyner Systemic hypoxia and vasoconstrictor responsiveness in exercising human muscle J Appl Physiol, November 1, 2006; 101(5): 1343 - 1350. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. P. Walsh and J. M. Marshall The early effects of chronic hypoxia on the cardiovascular system in the rat: role of nitric oxide J. Physiol., August 15, 2006; 575(1): 263 - 275. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. P. Walsh and J. M. Marshall The role of adenosine in the early respiratory and cardiovascular changes evoked by chronic hypoxia in the rat J. Physiol., August 15, 2006; 575(1): 277 - 289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Gonzalez-Alonso, S. P. Mortensen, E. A. Dawson, N. H. Secher, and R. Damsgaard Erythrocytes and the regulation of human skeletal muscle blood flow and oxygen delivery: role of erythrocyte count and oxygenation state of haemoglobin J. Physiol., April 1, 2006; 572(1): 295 - 305. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Casanello, A. Torres, F. Sanhueza, M. Gonzalez, M. Farias, V. Gallardo, M. Pastor-Anglada, R. S. Martin, and L. Sobrevia Equilibrative Nucleoside Transporter 1 Expression Is Downregulated by Hypoxia in Human Umbilical Vein Endothelium Circ. Res., July 8, 2005; 97(1): 16 - 24. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
