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Carbon monoxide promotes endothelium-dependent constriction of isolated gracilis muscle arterioles
Fruzsina K Johnson1, Robert A Johnson
1Dept. of Physiology, Tulane University Health Sciences Center, 1430 Tulane Ave., SL39, New Orleans, LA 70112, USA. Fruzsi123@aol.com
Insights
Carbon monoxide (CO) can cause blood vessels to constrict. This study found that CO promotes vasoconstriction by inhibiting nitric oxide (NO) formation in arterioles.
Area of Science:
- Physiology
- Vascular Biology
- Biochemistry
Background:
- Heme oxygenase metabolizes heme to carbon monoxide (CO) in vascular tissues.
- CO is known to relax vascular smooth muscle.
- CO also inhibits nitric oxide (NO) formation, suggesting complex roles in vascular function.
Purpose of the Study:
- To investigate the hypothesis that CO promotes endothelium- and NO synthase-dependent vasoconstriction.
- To elucidate the mechanism by which CO affects vascular tone in isolated arterioles.
Main Methods:
- Studies were performed on pressurized first-order gracilis muscle arterioles from Sprague-Dawley rats.
- Vascular responses to exogenous CO and delta-aminolevulinic acid (delta-ALA) were assessed with intact and removed endothelium.
- Effects of NO synthase inhibition (Nomega-nitro-l-arginine methyl ester) and NO donors were evaluated.
Main Results:
- Exogenous CO and delta-ALA induced vasoconstriction in arterioles with intact endothelium.
- These vasoconstrictions were abolished by endothelial removal.
- CO-induced vasoconstriction was converted to dilation by NO synthase inhibition and prevented by l-arginine, indicating inhibition of NO formation.
Conclusions:
- Exogenous and endogenously formed CO can promote endothelium-dependent vasoconstriction in isolated gracilis muscle arterioles.
- CO likely induces vasoconstriction by inhibiting endothelial nitric oxide (NO) formation.
- This finding reveals a novel mechanism for CO-mediated vascular regulation.
Abstract:
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.
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