Adrenaline increases the rate of cycling of crossbridges in rat cardiac muscle as measured by pseudo-random binary noise-modulated perturbation analysis

The mechanism of action of adrenaline on cardiac contractility in rat papillary muscles containing V₁ and V₃ isomyosins was analyzed during barium-activated contractures at 25°C by frequency domain analysis using pseudo-random binary noise-modulated perturbations. The analysis characterizes a frequency (f(min)) at which dynamic stiffness of a muscle is a minimum, a parameter that reflects the rate of cycling of crossbridges. We have previously shown that f(min) for V₁- and V₃-containing papillary muscles were 2.1 ± 0.2 Hz (mean ± SD) (n = 10) and 1.1 ± 0.2 Hz (n = 8), respectively, and that these values were independent of the level of activation. The present study's goal was to determine whether the inotropic action of adrenaline was associated with an increased rate of crossbridge cycling. The results show that a saturating dose of adrenaline increased f(min) in V₁ hearts by 49 ± 2% (n = 11). The action on V₃ hearts was significantly less; the increase in f(min) was 26 ± 2% (n = 6). The increase in f(min) for V₁ hearts was shown to be sensitive to the β-blocking agent propranolol. These results suggest that adrenaline significantly increases the rate of crossbridge cycling by a β-receptor-mediated mechanism. We conclude that the increased contractility of the heart in the presence of adrenaline arises not only from more complete activation of the contractile proteins but also from the increased rate at which each crossbridge can transduce energy.