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Prostacyclin (PGI2) dose-dependently increases the adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels in canine femoral, carotid, and canine and bovine coronary arteries. The prostacyclin-stimulation is enhanced by phosphodiesterase inhibitors, and is readily measurable after 60 sec incubation. The prostaglandin endoperoxide PGH2, but not PGH1, also elevates cAMP levels in femoral arteries. Inhibition of arterial prostacyclin synthetase with 28 microM 9,11-azoprosta-5,13-dienoic acid (azo analog I) blocks the PGH2-stimulation of cAMP accumulation. Azo analog I does not attenuate a direct PGI2 stimulation, indicating that the PGH2 dependent elevation of cAMP is due to conversion of PGH2 to PGI2 by the artery. PGI2 and PGE1 increase cyclic AMP levels and relax dog femoral and bovine coronary arteries, while PGE2, which actually contracts bovine coronary arteries, has no effect on arterial cyclic AMP levels. The significance of the PGI2-stimulation of arterial cyclic AMP is not known, but it is probably related to relaxation of arterial strips.
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