1: Am J Physiol Regul Integr Comp Physiol. 2003 Sep;285(3):R536-41. Epub 2003
Apr 3. 

Comment in:
    Am J Physiol Regul Integr Comp Physiol. 2003 Sep;285(3):R522-3.

Carbon monoxide promotes endothelium-dependent constriction of isolated gracilis
muscle arterioles.

Johnson FK, Johnson RA.

Dept. of Physiology, Tulane University Health Sciences Center, 1430 Tulane Ave.,
SL39, New Orleans, LA 70112, USA. Fruzsi123@aol.com

Vascular tissues express heme oxygenase, which 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 (delta-ALA), constricted
arterioles with intact endothelium pretreated with phenylephrine; these effects
were abolished by removal of the endothelium. CO- and delta-ALA-induced
vasoconstrictions were converted to dilations by pretreatment with an inhibitor
of NO synthase, Nomega-nitro-l-arginine methyl ester, or with
Nomega-nitro-l-arginine methyl ester and an 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. Because 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.

PMID: 12676757 [PubMed - indexed for MEDLINE]