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Temperature dependence of Na + −H + exchange, Na + −HCO 3 − co‐transport, intracellular buffering and intracellular pH in guinea‐pig ventricular myocytes
Author(s) -
Ch'en Frederick F.T.,
Dilworth Emma,
Swietach Pawel,
Goddard Ruth S.,
VaughanJones Richard D.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.051888
Subject(s) - intracellular ph , intracellular , chemistry , hepes , biophysics , analytical chemistry (journal) , nuclear chemistry , biochemistry , chromatography , biology
Almost all aspects of cardiac function are sensitive to modest changes of temperature. We have examined the thermal sensitivity of intracellular pH regulation in the heart. To do this we determined the temperature sensitivity of pH i , intracellular buffering capacity, and the activity of sarcolemmal acid‐extrusion proteins, Na + ‐H + exchange (NHE) and Na + ‐HCO 3 − co‐transport (NBC) in guinea‐pig isolated ventricular myocytes. pH i was recorded fluorimetrically with acetoxymethyl (AM)‐loaded carboxy‐SNARF‐1 at either 27 or 37°C. At 27°C, intrinsic (non‐CO 2 ‐dependent) buffering power (β i ) was ˜60 % of that at 37°C. Acid‐extrusion ( J e ) through NHE was ˜50 % slower than at 37°C, consistent with a Q 10 of ˜2. In 5 % CO 2 /HCO 3 − ‐buffered conditions, in the presence of 30 μ m cariporide to inhibit NHE, acid extrusion via NBC was also slowed at 27°C, suggestive of a comparable Q 10 . Resting pH i at 27°C was similar in Hepes‐ or 5 % CO 2 /HCO 3 − ‐buffered superfusates but, in both cases, was ˜0.1 pH units lower at 37°C. The higher the starting pH i , the larger was the thermally induced fall of pH i , consistent with a mathematical model where intrinsic buffers with a low principal p K a (e.g. close to 6.0) are less temperature‐sensitive than those with a higher p K a . The high temperature sensitivity of pH i regulation in mammalian cardiac cells has implications for experimental work conducted at room temperature. It also has implications for the ability of intracellular acidosis to generate intracellular Na + and Ca 2+ overload, cardiac injury and arrhythmia in the heart.