Abstract
When the guinea-pig ventricular muscle was exposed to hypertonic solution, duration of the action potential (APD) initially increased and then progressively decreased. To inverstigate the mechanism underlying this phenomenon, the preparations were perfused with the hypertonic solution under various experimental conditions. At low stimulus rates (0.1-l/min), the initial prolongation of APD was prominent while the later shortening of APD developed slowly, thereby suggesting that the effect of hypertonic solution on APD is dependent on the muscle activity. A pronounced shortening of APD occurred when the osmotic challenge was made at reduced [K]o (2mM-K), at reduced [Na]o (50%-Na), and at elevated [Ca]o (5.4mM-Ca). Lowering the temperature from 36 to 26-27°C nearly abolished the development of APD shortening. The resting potential and the maximum rate of rise (Vmax) of the action potential changed little even when APD was rapidly shortened during the osmotic challenge. Thus, the mechanism of APD shortening is thought to be independent of the factors determining the resting potential and Vmax. Mn ions (1-2mM), verapamil (5-10μM), and Ba ions (0.05-0.2mM) had no effect on the hypertonicity-induced changes in APD. In partially depolarized preparations, hypertonic solution increased the duration of Ca-dependent slow action potentials without producing any parallel increase in their upstroke velocity. It is postulated that the initial prolongation of APD in response to hypertonicity is a direct result of cell dehydration. The later shortening of APD is probably derived from certain changes in the cell condition which developed secondarily to the cell dehydration. In these changes in APD, the slow Ca current seems to play a small role.
