Sarcolemmal Na+/H+ exchanger activity and expression in human ventricular myocardium
Hiroyuki Yokoyama, MDa,
Suba Gunasegaram, BSca,
Sian E. Harding, PhD* and
Metin Avkiran, PhDa
a Center for Cardiovascular Biology and Medicine, Kings College London, London, United Kingdom
* National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom

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Figure 1 The relationship between pHi and ßi in human ventricular myocytes obtained from unused donor hearts (open symbols) and recipient hearts with end-stage heart failure (solid symbols). Linear least squares regression analysis of all points gave the equation ßi = 33.7·pHi + 260.1. ßi = intrinsic buffering power; pHi = intracellular pH.
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Figure 2 (A) Representative single-cell pHi recordings during acid pulses and (B) individual and mean JH6.9 values in ventricular myocytes obtained from unused donor hearts (open symbols) and recipient hearts with end-stage heart failure (solid symbols). In (B), n indicates the number of hearts in each group. pHi = intracellular pH; JH6.9 = rate of H+ efflux at pHi 6.90.
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Figure 3 Representative recordings of (A) pHi and (B) cell contraction in human ventricular myocytes from recipient hearts with end-stage heart failure during two consecutive acid pulses. The first acid pulses (open symbols) were under control conditions whereas during the second acid pulses (solid symbols) HOE-642 (1 µmol/L) was present during exposure to NH4Cl and the first 7 min of NH4Cl washout, as indicated by the horizontal bars. The baseline changes in (B) reflect changes in resting cell length. pHi = intracellular pH.
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Figure 4 Autoradiograms illustrating protein expression of (A) the Na+/H+ exchanger (NHE1 isoform) and (B) the Na+/Ca2+ exchanger in ventricular samples from unused donor hearts and recipient hearts with end-stage heart failure. Heart numbers relate to Table 1; in (B) the lane between heart numbers 10 and 13 contained size markers.
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