Role of an Electrogenic Na+-HCO3− Cotransport in Determining Myocardial pHi After an Increase in Heart Rate
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The contribution of electrogenic Na+-HCO3− cotransport to pHi regulation during changes in heart rate was explored in cat papillary muscles loaded with BCECF-AM in bicarbonate-free (HEPES) medium and in CO2/HCO3−-buffered medium. Stepwise increments in the frequency of contraction from 15 to 100 bpm induced a reversible increase in the pHi from 7.13±0.03 to 7.36±0.03 (P<.05, n=5) in the presence of CO2/HCO3− buffer. The same increase in the frequency of stimulation, however, decreased pHi from 7.10±0.02 to 6.91±0.06 (P<.05, n=5), in the absence of bicarbonate. Moreover, in CO2/HCO3−-superfused muscles pretreated with SITS (0.1 mmol/L), this effect of increasing the contraction frequency was reversed, and a decrease of pHi from 7.03±0.04 to 6.88±0.06 (P<.05, n=4) was observed when the pacing rate was increased stepwise from 15 to 100 bpm. High [K+]o–induced depolarization of cell membrane alkalinized myocardial cells in the presence of HCO3− ions, whereas acidification was observed as a consequence of hyperpolarization induced by low external [K+]o. Myocardial resting membrane potential became hyperpolarized upon exposure to HCO3−-buffered media. This HCO3−-induced hyperpolarization was not blocked by the inhibition of Na+,K+-ATPase activity by ouabain (0.5 μmol/L) but was prevented by SITS. The results suggested that membrane depolarization during cardiac action potential causes an increase in electrogenic Na+-HCO3− cotransport. Such depolarizations occurring as a consequence of increases in heart rate would thus, by means of elevated bicarbonate influxes, substantially increase the myocardial cell's ability to recover from an enhanced proton production.
- Received February 8, 1996.
- Accepted June 27, 1996.