EFFECT OF CARBACHOL AND NOREPINEPHRINE ON PHOSPHATIDYL-INOSITOL HYDROLYSIS AND CYCLIC-AMP LEVELS IN GUINEA-PIG URINARY-TRACT

Muscarinic cholinergic and adrenergic agonist-induced changes in [H-3] -phosphatidyl inositol (PI) hydrolysis and cyclic AMP (cAMP) levels we re measured in guinea pig ureter, urethra and bladder dome. In the ure ter, carbachol, norepinephrine and phenylephrine rapidly increased PI hydrolysis and basal cAMP levels, but did not decrease forskolin-stimu lated cAMP levels. In the bladder dome, norepinephrine and phenylephri ne produced a rapid but transitory increase in PI hydrolysis, but did not affect forskolin-stimulated cAMP levels. Carbachol produced a rapi d and sustained increase in PI hydrolysis and also, at high concentrat ions, decreased forskolin-stimulated cAMP levels. In the urethra, nore pinephrine and carbachol rapidly decreased forskolin-stimulated cAMP l evels and later increased PI hydrolysis. Our data suggest that the pre dominant second messenger system in the ureter, dome, or urethra is mo re dependent on the tissue than on the agonist. These tissue-specific, agonist-induced rapid changes in second messenger levels may help coo rdinate the contraction-relaxation phenomena necessary for urinary tra ct function.