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Modulation of transient outward current by extracellular protons and Cd 2+ in rat and human ventricular myocytes
Author(s) -
Stengl Milan,
Carmeliet Edward,
Mubagwa Kanigula,
Flameng Willem
Publication year - 1998
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 - 10.1111/j.1469-7793.1998.827bg.x
Subject(s) - acidosis , extracellular , myocyte , divalent , biophysics , chemistry , cardiac transient outward potassium current , patch clamp , medicine , endocrinology , biochemistry , biology , receptor , organic chemistry
1 The effects of extracellular acidosis and Cd 2+ on the transient outward current ( I to ) have been investigated in rat and human ventricular myocytes, using the whole‐cell patch‐clamp technique. 2 In rat myocytes, exposure to acidic extracellular solution (pH 6.0) shifted both steady‐state activation and inactivation curves to more positive potentials, by 20.5 ± 2.7 mV (mean ± s.e.m.; n = 4 ) and 19.8 ± 1.2 mV, respectively. Cd 2+ also shifted the activation and inactivation curves in a positive direction in a concentration‐dependent manner. 3 In human myocytes, the steady‐state activation and inactivation curves were located at more positive potentials. The effect of Cd 2+ was similar, but acidosis had less effect than in rat myocytes (e.g. pH 6.0 shifted activation by only 7.2 ± 2.2 mV and inactivation by 13.7 ± 0.5 mV; n = 4 ). 4 In both species, the effect of acidosis decreased with increasing concentrations of Cd 2+ and vice versa, suggesting competition between H + and Cd 2+ for a common binding site. 5 The data indicate that acidosis and divalent cations influence I to via a similar mechanism and act competitively in both rat and human myocytes, but that human cells are less sensitive to the effects of acidosis.