Journal of Applied Physiology, Vol 51, Issue 1 179-184, Copyright © 1981 by American Physiological Society
Adenosine and the acid-base state of vascular smooth muscle
R. A. Fenton, R. Rubio and R. M. Berne
Hog carotid artery media was incubated under conditions of normocapnia (95%
O2-5% CO2) and hypercapnia (nominally 75% O2-25%CO2). The intracellular pH
(pHi) was determined from the distribution of 14C-labeled
5,5-dimethyloxazoladine-2,4-dione, alpha- and beta-receptor antagonists
were used to block the effects of endogenous catecholamines. With 5% CO2,
adenosine had no effect on the pHi. High K+ (25mM) and dipyridamole (DPM)
induced a cellular metabolic acidosis that was reversed by adenosine and
not affected by 0.5 mM ca2+ or ouabain. Hypercapnia decreased the resting
pHi from 7.30 to 6.79. Adenosine significantly attenuated this decrease.
With high K+ or DPM, a similar degree of hypercapnia only depressed the pHi
to 6.91 and 6.90, respectively. The alkalinizing effect of high K+ and DPM
was not altered by 0.5 mM Ca2+, was partically reversed by ouabain, and was
completely reversed by adenosine. These results suggest that, under
normocapnic conditions, although adenosine relaxes the contraction
associated with K+-depolarization, it does not do so by elevating cellular
proton levels. However, adenosine may decrease a tissue's ability to
attenuate a local respiratory acidosis characteristic of increased O2
demand, resulting in relaxation under hypercapnic conditions. In any case,
this demonstrates an interaction, with respect to the acid-base state of
the vascular smooth muscle cells, among adenosine, K+, and H+, all
suggested components of the metabolic theory of blood flow autoregulation.
