| Literature DB >> 3093824 |
F L Belloni, S P Bruttig, R Rubio, R M Berne.
Abstract
We wanted to determine whether CO2, H+ and K+ affect the adenosine metabolism of vascular smooth muscle in a way that could account for the effects of these substances on vascular reactivity and their ability to modulate adenosine-induced vascular relaxation. Accordingly, 1-week-old cultures of rat aortic smooth muscle were incubated in phosphate-buffered saline with various [K+]'s and pH's and aerated in an incubation chamber with gases containing various proportions of CO2. Uptake was measured as 14C incorporation into cellular constituents during exposure to 2 microM [14C]adenosine. Release was measured as net extracellular adenosine accumulation. Uptake of adenosine was not significantly affected by any of the experimental maneuvers, except that it was greatly attenuated by dipyridamole (10(-5) and 10(-4) M) and transiently enhanced by the low CO2 levels. Adenosine release, however, was depressed by lowering atmospheric CO2 (0% vs 5%) and also by normocapnic acidosis (pH 6.8 vs pH 7.4). We conclude that vascular smooth muscle in culture releases adenosine at a rate that might have vasoactive significance in vivo. Furthermore, some of the vascular actions of CO2 and H+, but not those of K+, may be partially explained by their effects on vascular smooth muscle's adenosine metabolism.Entities:
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Year: 1986 PMID: 3093824 DOI: 10.1016/0026-2862(86)90054-3
Source DB: PubMed Journal: Microvasc Res ISSN: 0026-2862 Impact factor: 3.514