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Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131-5218
Chronic hypoxic
exposure has been previously demonstrated to attenuate systemic
vasoconstrictor activity to a variety of agents. This attenuated
responsiveness is observed not only in conscious animals but in
isolated vascular preparations as well. Because hypoxia has been
documented to increase heme oxygenase (HO) levels and the subsequent
production of the vasodilator CO in vitro, we hypothesized that the
blunted reactivity observed with chronic hypoxia (CH) may be in part
due to increased HO activity. In thoracic aortic rings from CH rats,
cumulative dose-response curves to phenylephrine (PE) in the presence
of the nitric oxide (NO) synthase inhibitor
N
-nitro-L-arginine
(L-NNA) and the HO inhibitor
zinc protoporphyrin 9 (ZnPPIX) elicited increased contractility
compared with CH rings treated with only
L-NNA. Similar results were
observed in rings incubated overnight with the HO-inducing agent sodium
m-arsenite. In contrast, contractile
responses in rings from control rats were unaffected by the HO
inhibitor. Furthermore, endothelium-denuded rings from either control
or CH rats did not exhibit an increase in reactivity to PE following
ZnPPIX incubation. ZnPPIX had no effect on relaxant responses to the NO
donor
S-nitroso-N-penicillamine, suggesting that its actions were specific to HO inhibition. Finally, aortic rings exhibited dose-dependent relaxant responses to exogenous CO that were endothelium independent and blocked by an inhibitor of
soluble guanylyl cyclase. The other products of HO enzyme activity, iron and biliverdin, were without effect on vasoreactivity. Thus we
conclude that the attenuated vasoreactivity to PE following CH is
likely to involve the induction of endothelial HO and the subsequent
enhanced production of CO.
rat; thoracic aorta; heme oxygenase; nitric oxide synthase; endothelium
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