Isoproterenol enhances myocardial relaxation more than contraction, likely mediated by the protein kinase system, distinguishing its inotropic profile from calcium.
Suggests lusitropic selectivity of beta-agonists in animal myocardium; leaves open translation to human HF therapy.
The relaxing effect of two positive inotropic interventions was studied in the isolated rat heart beating at constant rate and perfused at constant coronary flow. Experiments were performed under isotonic or isometric conditions during heart perfusions with Ca2+, 3.5 X 10(-3) M, and with isoproterenol, 10(-7) to 10(-8) M. Changes induced in maximal velocity of contraction (+L or +T) and maximal velocity of relaxation (-L or -T) were analyzed as the ratio between both maximal velocities (+L/-L or +T/-T). For similar increments in the amount of the apex-to-base shortening or in developed tension during Ca2+ or isoproterenol perfusions, the effect on the maximal velocity of relaxation differed for each intervention. High Ca2+ perfusion increased velocities of contraction and relaxation proportionally without significant changes in their ratio. Isoproterenol increased -L or -T more than +L or +T and the ratio showed a significant fall both in isotonic and isometric experiments (+L/-L, -0.33 +/- 0.11 and +T/-T, -0.38 +/- 0.09; P less than 0.01). The relaxing effect of the beta agonist seems to be related to the activation of the protein kinase system since perfusions with dibutyryl 3',5'-cAMP had a greater effect on the relaxation of the hearts.
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Gende et al. (1977) studied this question.
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