Augmentation by external Mg ions of beta-adrenoceptor-mediated actions in the longitudinal muscle of rat uterus.

1. The longitudinal muscle isolated from the uterus of oestrogen-treated rats was not spontaneously active in Locke solution, and electrical stimulation evoked phasic contraction. Isoprenaline (3 x 10(-11) - 10(-8) M) and dibutyryl cyclic AMP (db cyclic AMP, 0.1-0.8 mM) depressed the phasic contraction; the depression was enhanced in the presence of 0.6 mM Mg. 2. The contracture generated by 40 mM K was partially relaxed by isoprenaline (10(-11) - 10(-8) M) and db cyclic AMP (0.1-0.8 mM). Mg (0.6 mM) enhanced the isoprenaline-induced relaxation, but not that induced by db cyclic AMP. 3. The membrane potential of the muscle was -61 mV, and electrical stimulation induced an action potential which consisted of spike and plateau components. Application of isoprenaline and db cyclic AMP mainly reduced the duration of the plateau potential. The effect was potentiated by 0.6 mM Mg. 4. The membrane was hyperpolarized, accompanied by a decrease in membrane resistance, when 10(-8) M isoprenaline or 0.8 mM db cyclic AMP was applied. The effects of isoprenaline were prominently augmented in the presence of 1.2 mM Mg, while those of db cyclic AMP were slightly potentiated. 5. Forskolin (0.1 microM) or papaverine (10 microM) inhibited the phasic contraction and the K-contracture. The effect on the phasic contraction was potentiated by 0.6 mM Mg, while that on the K-contracture was not affected. 6. Forskolin shortened the action potential at 0.3 microM, and hyperpolarized the membrane with a decrease in membrane resistance at 3.0 microM. The membrane effects were augmented by 0.6 and 1.2 mM Mg, respectively. 7. It was hypothesized that external Mg ions could affect at least two processes involved in actions at beta-adrenoceptors on rat myometrium; receptor-agonist interaction and cyclic AMP-mediated inhibition of membrane excitability.