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Prostacyclin increases cAMP in coronary arteries
Journal of Cyclic Nucleotide Research
|December 1, 1979
Summary
Prostacyclin (PGI2) causes coronary artery relaxation by increasing cyclic adenosine monophosphate (cAMP) levels. This mechanism, mediated by cAMP, is similar to that of isoprenaline and adenosine.
Area of Science:
- Cardiovascular Pharmacology
- Molecular Cardiology
Background:
- Prostacyclin (PGI2) is a vasodilator with known effects on coronary arteries.
- The intracellular signaling pathways mediating PGI2-induced relaxation are not fully elucidated.
Purpose of the Study:
- To investigate whether cyclic adenosine monophosphate (cAMP) mediates prostacyclin (PGI2)-induced relaxation in bovine coronary arteries.
- To compare the effects of PGI2 on cAMP and cyclic guanosine monophosphate (cGMP) levels with its relaxant effects.
Main Methods:
- Circular strips of partially depolarized bovine coronary arteries were used.
- PGI2-induced changes in arterial strip length were measured.
- Tissue concentrations of cAMP and cGMP were quantified using radioimmunoassay (RIA).
Main Results:
- PGI2 caused significant, concentration-dependent increases in cAMP levels.
- These cAMP increases were closely associated with PGI2-induced relaxation.
- PGI2 did not alter cGMP levels, and its relaxant effects were not blocked by propranolol.
- A strong linear correlation was observed between elevated cAMP and percent relaxation.
Conclusions:
- The findings suggest that prostacyclin (PGI2)-induced relaxation of coronary arteries is mediated by cyclic adenosine monophosphate (cAMP).
- This cAMP-dependent mechanism is analogous to the relaxation pathways activated by isoprenaline and adenosine.