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1 Department of Physiology, Tulane University Health Sciences Center, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: Fruzsi123{at}aol.com.
Vascular tissues express heme oxygenase that metabolizes heme to form carbon monoxide (CO). CO promotes relaxation of vascular smooth muscle, but also inhibits nitric oxide (NO) formation. This study examines the hypothesis that CO promotes endothelium- and NO synthase-dependent vasoconstriction of isolated arterioles. Studies were conducted on pressurized first-order gracilis muscle arterioles isolated from anesthetized male Sprague-Dawley rats. Exogenous CO, as well as a heme precursor, delta-aminolevulinic acid (
-ALA) constricted arterioles with intact endothelium pretreated with phenylephrine; these effects were abolished by endothelium removal. CO and -ALA-induced vasoconstrictions were converted to dilations by pretreatment with an inhibitor of NO synthase, N
-nitro-L-arginine methyl ester (L-NAME) or by pretreatment with L-NAME and a NO donor, sodium nitroprusside. Furthermore, CO-induced vasoconstriction was prevented by pretreatment with the NO synthase substrate, L-arginine. This study shows that exogenous, as well as endogenously-formed CO can promote endothelium-dependent vasoconstriction in isolated gracilis muscle arterioles. Since CO-induced vasoconstriction is abolished by NO synthase blockade and by L-arginine, CO most likely promotes endothelium-dependent vasoconstriction by inhibiting endothelial NO formation.
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