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1 Department of Cell Biology and Physiology, University of New Mexico, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: bwalker{at}salud.unm.edu.
Chronic hypoxia (CH) is associated with both blunted agonist-induced and myogenic vascular reactivity; possibly due to an enhanced production of heme oxygenase (HO) derived carbon monoxide (CO). However, the mechanism of endogenous CO-meditated vasodilation remains unclear. Isolated pressurized mesenteric arterioles from CH rats (48 hr @ PB = 380 torr) were pre-constricted with phenylephrine and administered the substrate for HO, heme-L-lysinate (HLL) in the presence or absence of the large conductance Ca2+-activated K+ channel (BK) inhibitor iberiotoxin, the sGC inhibitor ODQ, ryanodine-sensitive Ca2+ channel blockade (ryanodine), or free radical spin-traps (PBN and tiron). In addition, the effect of HLL administration on vascular smooth muscle (VSM) membrane potential was assessed in superior mesenteric artery strips in the presence and absence of HO inhibition or iberiotoxin. The vasodilatory response to exogenous CO was assessed in the presence and absence of ODQ or iberiotoxin. The vasodilatory response to biliverdin was also assessed in arteries from control and CH rats and in arteries from CH rats in the presence and absence of iberiotoxin. HLL administration produced a dose-dependent vasodilatory response, which was nearly eliminated in the presence of iberiotoxin. Neither ODQ, spin-traps, or ryanodine altered the vasodilatory response to HLL, although ODQ abolished the vasodilatory response to SNAP. HLL administration produced a ZnPPIX- and iberiotoxin-sensitive VSM cell hyperpolarization. Iberiotoxin and ODQ inhibited the vasodilatory response to exogenous CO. Biliverdin produced a dose-dependent vasodilatory response in arteries from both control and CH rats, which was insensitive to iberiotoxin. In conclusion, the vasodilatory response to endogenous CO involves cGMP-independent activation of VSM cell BK channels that does not likely involve the formation of Ca2+-sparks emanating from ryanodine-sensitive stores.
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