RELATIONSHIP BETWEEN INTRACELLULAR PH AND TENSION DEVELOPMENT IN RESTING VENTRICULAR MUSCLE AND MYOCYTES

Simultaneous measurements of intracellular pH (pH(i)) and tension development were made in resting cat papillary muscles and resting ventricular myocytes (cat, guinea pig). pH microelectrodes and the fluorescent indicator carboxy-seminaphthorhodafluor-1 (SNARF-1) were used to measure pH(i) in muscles and myocytes, respectively. pH(i)-induced changes in isometric muscle tension and myocyte length were elicited by variations in PCO2, HCO3-, and [NH4Cl]. Increased pH(i) elevated resting tension and decreased resting cell length, whereas decreased pH(i) decreased tension and increased cell length. The tension-pH(i) and cell length-pH(i) relationships were nonlinear and displayed hysteresis. A reduction in extracellular [Ca2+] from 2.7 to 0.5 mM caused little or no change in the tension and cell length responses to elevated pH(i). Ca2+ uptake and/or release by the sarcoplasmic reticulum (SR) does not appear to be involved in the tension response to intracellular alkalosis because the response was unaffected by a postpacing rest period and was not inhibited by ryanodine (5-mu-M), which depletes SR Ca2+ stores. The cross-bridge inhibitor 2,3-butanedione monoxime (15 mM), but not internal dialysis with 14 mM ethylene glycol-bis(beta-aminoethyl ether) N,N, N',N'-tetraacetic acid, inhibited myocyte contractures elicited by elevated pH(i). The latter finding suggests that factors other than pH(i)-induced increase in myofilament Ca2+ sensitivity may contribute to the resting contractile response to elevated pH(i).