Abstract
Contraction and relaxation in mammalian cardiac muscle are regulated by the change in intracellualr Ca2+ concentration ( [Ca2+] i) and modified by neurotransmitters. The aim of the present study was to clarify the effects of beta-receptor stimulation on intracellular Ca transients and tension in ferret ventricular muscle. To monitor the Ca transients, aequorin was micro-injected into superficial cells of the preparation and the resultant light signal and tension were simultaneously recorded. Isoproterenol (Iso) increased the peaks of Ca transients and tension, and shortened the decay time of Ca transients. Relaxation time was slightly shortened by Iso, but this was not statistically significant. The time required to reach peak tension and peak light was shortened. Relation between [Ca2+] i and tension obtained by tetanic contraction, produced by repetitive stimulation in the presence of ryanodine, was shifted to the right by Iso. However, maximal tension was slightly enhanced by Iso. The results were interpreted as follows : Beta-receptor stimulation potentiates tension by increasing the Ca transient peak, but the maximal tension was not dramatically changed. The main factor determining relaxation might not be the Ca uptake rate by sarcoplasmic reticulum, or Ca sensitivity change of the contractile element.
