Lusitropic effects of alpha- and beta-adrenergic stimulation in amphibian heart.

The effects of beta and alpha-adrenergic stimulation in amphibian superfused hearts and ventricular strips were studied. Superfusion with 3 x 10(-8) M isoproterenol produced a positive inotropic effect, as detected by a 92 +/- 24% increase in the maximal rate of contraction (+T) and a positive lusitropic effect characterized by a decrease in both the ratio +T/-T (23 +/- 5%) and the half relaxation time (t1/2) (19 +/- 4%). The mechanical behavior induced by the beta-agonist was associated with an increase in the intracellular cAMP levels from control values of 173 +/- 19 to 329 +/- 28 nmol/mg wet tissue. Hearts superfused with 32P in the presence of isoproterenol showed a significant increase in Tn 1 phosphorylation (from 151 +/- 13 to 240 +/- 44 pmol 32P/mg MF protein) without consistent changes in phosphorylation of C-protein. In sarcoplasmic reticulum membrane vesicles, no phospholamban phosphorylation was detected either by beta-adrenergic stimulation of superfused hearts or when phosphorylation conditions were optimized by direct treatment of the vesicles with cAMP-dependent protein kinase (PKA) and [gamma 32P] ATP. The effect of alpha-adrenergic stimulation on ventricular strips was studied at 30 and 22 degrees C. At 30 degrees C, the effects of 10(-5) to 10(-4) M phenylephrine on myocardial contraction and relaxation were diminished to non significant levels by addition of propranolol. At 22 degrees C, blockage with propranolol left a remanent positive inotropic effect (10% of the total effect of phenylephrine) and changed the phenylephrine-induced positive lusitropic effect into a negative lusitropic action.(ABSTRACT TRUNCATED AT 250 WORDS)