beta-Adrenergic relaxation and cAMP kinase activation in coronary arterial smooth muscle

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Abstract
If .beta.-adrenergic relaxation of smooth muscle is partly mediated by the cAMP system, then .beta.-stimulation should be correlated to activation of cAMP-dependent protein kinase (cPK). Studies were performed with bovine coronary arterial strips to identify isozymic forms of cPK and to determine if .beta.-relaxation is correlated to activation of cPK (reflected by elevated ratios of cPK activity without cAMP to cPK activity with cAMP). Both ion exchange chromatography and a new electrophoretic technique revealed 2 cPK isozymes (types I and II). No change in cPK activity occurred in strips contracted with 30 mM KCl. Dose- and time-dependent relaxation during .beta.-stimulation with isoproterenol was highly correlated to parallel increases in cPK activity. Increased cPK activity was inhibited in assays performed with a specific inhibitor of cPK. Both relaxation and activation of cPK were abolished during .beta.-adrenergic blockade with propranolol. Relaxation by KCl removal or the ionophore Ro2-2985 [lasalocid], unlike .beta.-mediated relaxation, did not increase cPK activity. .beta.-Mediated relaxation of isolated coronary arterial strips specifically activates cPK, and the hypothesis that .beta.-induced relaxation of vascular smooth muscle involves the cAMP system is supported.