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Articles in PresS, published online ahead of print June 13, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00125.2002
Submitted on February 21, 2002
Accepted on June 6, 2002
1 Cell Biology & Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: searley{at}salud.unm.edu.
Blunted agonist-induced vasoconstrictor responsiveness following chronic hypoxia (CH) is associated with endothelium-dependent vascular smooth muscle (VSM) cell hyperpolarization and decreased vessel wall [Ca2+]. We hypothesized that myogenic vasoconstriction and pressure-induced Ca2+ influx would also be attenuated for vessels from CH rats. Mesenteric resistance arteries isolated from CH (PB=380 torr; 48 hours) or normoxic control (PB=630 torr) rats were cannulated and pressurized. VSM cell resting membrane potential was recorded via microelectrode at intraluminal pressures between 40 and 120 torr under normoxic conditions. VSM cells in vessels isolated from CH rats were hyperpolarized compared to controls at all pressures. Resistance arteries were loaded with the Ca2+ indicator fura-2AM and subjected to a series of intraluminal pressure steps (20-120 torr). Inner diameter was well maintained for vessels from control rats whereas vessels from CH rats developed less tone as pressure was increased. Pressure-induced increases in vessel wall [Ca2+] were also attenuated for resistance arteries from CH rats. Endothelium removal restored myogenic constriction to vessels from CH rats and normalized VSM cell resting membrane potential and pressure-induced Ca2+ responses to control levels. Myogenic constriction and pressure-induced vessel wall [Ca2+] increases remained blunted in the presence of the nitric oxide (NO) synthase inhibitor N
-nitro-L-arginine for endothelium-intact resistance arteries isolated from CH rats. We conclude that blunted myogenic reactivity following CH results from a non-NO endothelium-dependent VSM cell hyperpolarizing influence.
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