Am J Physiol Cell Physiol AJP: Lung Cellular and Molecular Physiology
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Am J Physiol Cell Physiol 262: C316-C327, 1992;
0363-6143/92 $5.00
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AJP - Cell Physiology, Vol 262, Issue 2 C316-C327, Copyright © 1992 by American Physiological Society

ARTICLES

Relationship between intracellular pH and tension development in resting ventricular muscle and myocytes

K. W. Spitzer and J. H. Bridge
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City 84112.

Simultaneous measurements of intracellular pH (pHi) 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 pHi in muscles and myocytes, respectively. pHi-induced changes in isometric muscle tension and myocyte length were elicited by variations in PCO2, HCO3-, and [NH4Cl]. Increased pHi elevated resting tension and decreased resting cell length, whereas decreased pHi decreased tension and increased cell length. The tension-pHi and cell length-pHi 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 pHi. 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 microM), 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 pHi. The latter finding suggests that factors other than pHi-induced increase in myofilament Ca2+ sensitivity may contribute to the resting contractile response to elevated pHi.


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