1. In isometrically contracting kitten papillary muscles, dibutyryl cyclic AMP (DBcAMP) enhanced peak tension, increased rates of contraction and relaxation, decreased tension of a phasic but not of a small tonic component of KCl-contractures, and caused aftercontractions. These effects resemble closely those of catecholamines. 2. The effects of DBcAMP on kitten papillary muscle were not influenced by (-)-bupranolol, a beta-adrenoceptor antagonist. 3. DBcAMP decreased KCl-contractures in strips of frog ventricle. 4. Phasic KCl-contractures in kitten papillary muscles were decreased by (-)- and (+)-isoprenaline. For similar effects, 100-fold higher concentrations of (+)-isoprenaline than of (-)-isoprenaline were required. 5. Increases in maximum rates of contraction and relaxation, increases in peak tension of isometric contractions and reduction of phasic KCl-contractures by catecholamines were antagonized competitively to a similar extent by (-)-bupranolol. Mean apparent equilibrium constants for the beta-adrenoceptor-(-)-bupranolol complex of 0.46-0.70 nM were estimated. These constants were quite similar irrespective of whether (-)-isoprenaline, (+)-isoprenaline or (-)-noradrenaline were used as agonists. 6. Increases in contractile strength, maximum rates of contraction and of relaxation of isometric contractions and decreases in KCl-contractures by (-)-isoprenaline were surmountably blocked by (+)-bupranolol. Mean apparent equilibrium constants for the receptor-(+)-bupranolol complex were 40-50 nM. 7. The equilibrium constants of (-)- and (+)-bupranolol for the receptors mediating positive inotropic and relaxant effects of catecholamines were not significantly different from constants for bupranolol-receptor complexes in cell-free membrane particles of kitten heart ventricle. It is suggested that the same beta-adrenoceptor triggers positive inotropic, relaxant and adenylyl cyclase-activating effects of catecholamines in kitten papillary muscle. 8. The partial agonist (-)-dichloroisoprenaline (DCI) (1 muM) reduced by 79% the phasic KCl-contractures of the kitten papillary muscles. DCI stimulates adenylyl cyclase activity of ventricle membranes to less than 1/4 of maximum stimulation by (-)-isoprenaline. If cyclic AMP produced by DCI is involved in the decrease of phasic KCl-contracture, small increase in cyclic AMP should be sufficient to induce this effect.
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