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Department of Pharmacology, School of Medicine, University of Miami, Miami, FL 33101, U.S.A.

1. The effects of isoprenaline (10^-6 M) on relaxation, unidirectional as well as net Ca²⁺ fluxes, and cyclic AMP levels were investigated in rabbit aorta under the condition of high-K⁺ depolarization in the presence of phentolamine (10^-5 M).

2. Isoprenaline (10^-6 M) caused significant inhibition of Ca²⁺ influx stimulated by 145 mM-K⁺ (0 Na⁺) solution. The time courses of Ca²⁺ influx inhibition and relaxation by isoprenaline were parallel. Isoprenaline also caused a significant inhibition of high-K⁺-induced gain in net Ca²⁺ content.

3. Ro 20-1724 (1 mM), a phosphodiesterase inhibitor, also caused relaxation and Ca²⁺ influx inhibition in high-K⁺-depolarized rabbit aorta. Pre-treatment with Ro 20-1724 potentiated isoprenaline-induced Ca²⁺ influx inhibition and relaxation.

4. Isoprenaline and Ro 20-1724 each alone increased cyclic AMP levels. Furthermore pre-treatment with Ro 20-1724 caused potentiation of isoprenaline-induced increases in cyclic AMP levels.

5. At submaximal concentration, D600 (10^-7 M) caused partial inhibition of high-K⁺-stimulated Ca²⁺ influx and produced relaxation. However, unlike Ro 20-1724, it did not potentiate isoprenaline-induced Ca²⁺ influx inhibition and relaxation. D600 does not increase cyclic AMP levels in smooth muscle.

6. Dibutyryl cyclic AMP (1 mM), a lipid-soluble analogue of cyclic AMP, caused relaxation and inhibited high-K⁺-stimulated Ca²⁺ influx.

7. Isoprenaline failed to cause stimulation of Ca²⁺ efflux in high-K⁺-depolarized rabbit aorta.

8. It is concluded that the inhibition of Ca²⁺ influx may be one of the mechanisms by which -receptor stimulation can reduce intracellular free Ca²⁺ to promote relaxation of smooth muscle. The data support the involvement of cyclic AMP in this action of the -agonist.

9. Since the experiments were conducted in 145 mM-K⁺ (0 Na⁺) depolarizing conditions, the role of hyperpolarization or of a Na⁺—Ca²⁺ exchange mechanism in isoprenaline-induced Ca²⁺ influx inhibition and/or relaxation can be excluded.

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