Korean J Physiol Pharmacol.
2001 Feb;5(1):87-92.
Effect of heme oxygenase induction by NO donor on the aortic contractility
- Affiliations
-
- 1College of Pharmacy, Sungkyunkwan University, Suwon, South Korea.
sylee@skku.ac.kr
Abstract
- Carbon monoxide (CO) binds to soluble guanylate cyclase to lead its
activation and elicits smooth muscle relaxation. The vascular tissues
have a high capacity to produce CO, since heme oxygenase-2 (HO-2) is
constitutively expressed in endothelial and smooth muscle cells, and
HO-1 can be greatly up-regulated by oxidative stress. Moreover, the
substrate of HO, heme, is readily available for catalysis in vascular
tissue. Although the activation of heme oxygenase pathway under various
stress conditions may provide a defence mechanism in compromised
tissues, the specific role of HO-1-derived CO in the control of aortic
contractility still remains to be elucidated. The present study was
done to determine the effect of HO-1 induction on the aortic
contractility. Thus, the effects of incubation of aortic tissue with
S-nitroso-N-acetylpenicillamine (SNAP) for 1 hr on the aortic
contractile response to phenylephrine were studied. The preincubation
with SNAP resulted in depression of the vasoconstrictor response to
phenylephrine. This effect was restored by HO inhibitor or methylene
blue but not by NOS inhibitor. The attenuation of vascular reactivity
by preincubation with SNAP was also revealed in endothelium-free rings.
AlF4--evoked contraction in control did not differ from that in
SNP-treated group. These results suggest that increased production of
CO was responsible for the reduction of the contractile response to
phenylephrine in aortic ring preincubated with SNAP and this effect of
SNAP was independent on endothelium.