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Purinoceptor mediated stimulation of prostacyclin release in the porcine pulmonary vasculature.

By P. G. Hellewell and J. D. Pearson

Abstract

Prostacyclin (PGI2) release from the piglet isolated perfused lung was measured by radioimmunoassay of 6-keto-PGF1 alpha in the venous effluent. Basal release of PGI2 was transiently stimulated up to 30 fold, in a dose-dependent manner, by bolus injections of ATP (0.03-3 mumol). A continuous infusion of ATP also produced a transient response. Dose-response curves for purinergic stimulation of PGI2 release showed that ADP was equipotent with ATP, while AMP and adenosine were virtually inactive. The non-hydrolyzable ATP analogue, ATP-gamma-S, elicited PGI2 release of similar magnitude and duration to that of ATP, suggesting that pulmonary catabolism of ATP is not required to induce PGI2 release. The results suggest that the porcine pulmonary vasculature possesses P2-purinoceptors through which the synthesis and release of PGI2 can be mediated

Topics: Research Article
Publisher: Nature Publishing Group
OAI identifier: oai:pubmedcentral.nih.gov:1987114
Provided by: PubMed Central
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