Sodium/calcium exchange and intracellular calcium buffering in ferret myocardium: an ion-sensitive micro-electrode study.

Measurements of the intracellular activity of Ca (aiCa), Na (aiNa) and H (pHi) ions have been made with resin-filled ion-sensitive micro-electrodes in ferret ventricular trabeculae. The mean values in quiescent muscle at 30 degrees C were: aiNa, 11.1 +/- 1.0 mM; aiCa, 58.4 +/- 6.4 nM, and pHi, 7.20 +/- 0.11. The relation between aiNa and extracellular Na activity (aoNa) is not linear and is sensitive to temperature: the Q10 for the change in aiNa in normal Tyrode solution is 1.3 +/- 0.5 and rises to 3.5 +/- 0.5 when aoNa is reduced to 1.1 mM. The addition of CN to the bathing fluid causes little or no change in aiNa or aiCa but pHi rises to 7.38 +/- 0.10, yet in some preparations resting tension increases. Similar results are seen with carbonyl cyanide m-chlorophenyl hydrazone. On lowering [Na]o, the fall in aiNa is very much greater than the rise in aiCa and the pHi is generally unchanged. When [Na]o is lowered in the presence of a respiratory inhibitor, the fall in aiNa is reduced, the rise in aiCa and the contracture tension are increased while pHi falls. The apparent coupling ratio for the Na/Ca exchange varies between 3 and 4 depending on the experimental conditions. These results suggest that an intracellular process, with a high Q10 and which depends upon respiration and aiNa, is able to remove Ca2+ from the sarcoplasm and thereby interact with the sarcolemmal Na/Ca exchange. This process could be the increase in the energy-dependent accumulation of Ca2+ within mitochondria that will occur when the Ca efflux from these organelles is progressively inhibited as aiNa falls.