Role of Ca in isoproterenol-induced increases in cAMP levels in rat uterus

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Abstract
The influence of alteration in the Ca2+ environment of the tissue on isoproterenol-induced increases in c[cyclic]AMP levels and relaxation was studied in rat uterus. In muscles depolarized with 47.5 mM K+ (with or without Na+), the ability of isoproterenol to increase cAMP levels and to produce relaxation was inversely related to external Ca concentration. The pretreatment of the muscle with D600 [methoxyverapamil] or EGTA [ethylene glycol bis(.beta.-aminoethyl ether) N,N,N'',N''-tetraacetic acid] restored the cAMP response to isoproterenol in the depolarized uterus to a level observed in nondepolarized muscle. The study with Ro 20-1724 [4-3-butoxy-4-methoxybenzyl)-2-imidazolidinone], a phosphodiesterase (PDE) inhibitor indicated that the failure of isoproterenol to elevate cAMP levels in the depolarized uterus could not be related to the activation of PDE by Ca2+. The exposure of rat uterus to a zero-Ca2+ solution accentuated the increases in cAMP levels produced by isoproterenol. Ca2+ may play a regulatory role in .beta.-androceptor-induced increases in cAMP levels in uterine smooth muscle.

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