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Vol. 285, Issue 3, 975-982, June 1998
Department of Allergy and Respiratory Medicine, UMDS Smooth Muscle
Group, UMDS, St Thomas' Campus, London SE1 7EH, United Kingdom
Chronic hypoxia is associated with altered pulmonary vasoreactivity,
and it has been suggested that an increased response to
voltage-dependent vasodilators may relate to enhanced Ca++
entry via voltage-dependent channels, secondary to
depolarization. Few studies have been performed on small pulmonary
arteries, and it is unknown whether they are depolarized after chronic
hypoxia. We examined the resting membrane potential, and the actions of voltage-dependent (verapamil, levcromakalim) and -independent (isoproterenol, forskolin, papaverine) vasodilators in small (~300 µm internal diameter) pulmonary arteries from chronically hypoxic rats. The resting membrane potential was more positive in arteries after chronic hypoxia (control: 
60 ± 0.5 mV; hypoxic:
54.4 ± 1.1 mV; P < .01), and this was reflected by a
shift to the left of the response curves for K+ and
4-aminopyridine. In arteries constricted with prostaglandin F2
the response to verapamil and
levcromakalim was increased after chronic hypoxia, although maximum
prostaglandin F2-induced tension was
unchanged, which implies a reduction in voltage-independent constrictor
mechanisms. Although vasorelaxation to isoproterenol was depressed in
arteries from hypoxic rats, forskolin-induced relaxation was enhanced
substantially, and because the response to the phosphodiesterase
inhibitor papaverine was unchanged, we suggest that this reflects an
up-regulation of adenylate cyclase. In conclusion, chronic hypoxia
resulted in a significant depolarization in small pulmonary arteries,
but this may explain only partly the increased efficacy of
voltage-dependent vasodilators. Whether the reduction in
voltage-independent constrictor mechanisms is related to the apparent
up-regulation of adenylate cyclase remains to be elucidated.
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