The effects of the transmembrane calcium and sodium gradients and membrane potential upon the contraction in frog atrial muscle.

A widely accepted view of excitation-contraction in heart muscle is, that depolarization causes voltage dependant calcium channels to open and calcium to flow into the cell. This calcium probably contributes partly to contraction but may cause the release of calcium from the sarcoplasmic reticulum (S.R.). Relaxation may be due to a re-uptake of calcium into the S.R. but an involvement of the Na-Ca exchange is apparent, from the immediate and dramatic effects of changes to [Na]o or [Ca]o, particularly in amphibian cardiac muscle. In this study, I have set out to investigate the characteristics of the Na-Ca exchange and its possible contribution to contraction and relaxation, in frog atrial trabeculae, using a double-sucrose gap, voltage clamp technique. The contracture studies show that the tonic component of tension is highly sensitive to Cao and Nao and is probably generated by the sarcolemmal Na-Ca exchange which is electro- genic in nature, with a coupling ratio of 3Na+ per 1Ca2+. The contribution of the exchange to the normal beating heart is likely to be greater in frog than mammals because of the reduced amount of S.R, the larger surface to volume ratio, hence less diffusion delay and a much higher intracellular Na concentration. It is also evident from my work, that the Na-Ca exchange is also involved with the relaxation process, the rate of relaxation being sensitive to Cao, and Nao and membrane potential, in a manner similar to the tonic tension. These results are discussed in terms of modified view of the cyclic nature of contraction and relaxation, incorporating the sarcolemmal Na-Ca exchange.