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Articles in PresS, published online ahead of print March 22, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00104.2002
Submitted on February 19, 2002
Accepted on March 12, 2002
1 Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: searley{at}unm.edu.
Chronic hypoxia (CH) results in reduced sensitivity to vasoconstrictors in conscious rats that persists upon restoration of normoxia. We hypothesized that this effect is due to endothelium-dependent hyperpolarization of vascular smooth muscle (VSM) cells following CH. VSM cell resting membrane potential was determined for superior mesenteric artery strips isolated from CH rats (PB = 380 torr; 48 hours) and normoxic controls. VSM cells from CH rats studied under normoxia were hyperpolarized compared to controls. Resting vessel wall calcium concentration ([Ca2+]), and pressure-induced vasoconstriction were reduced in vessels isolated from CH rats compared to controls. Vasoconstriction and increases in vessel wall [Ca2+] in response to the 
1-adrenergic agonist phenylephrine (PE) were also blunted in resistance arteries from CH rats. Removal of the endothelium normalized resting membrane potential, resting vessel wall [Ca2+], pressure-induced vasoconstrictor responses, and PE-induced constrictor and Ca2+ responses between groups. Whereas VSM cell hyperpolarization persisted in the presence of nitric oxide synthase inhibition, heme oxygenase inhibition restored VSM cell resting membrane potential in vessels from CH rats to control levels. We conclude that endothelial-derived carbon monoxide accounts for persistent VSM cell hyperpolarization and vasoconstrictor hyporeactivity following chronic hypoxia.
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