ABSTRACT
<p><b>AIM</b>To elucidate the possible mechanisms underlying antiarrhythmia of the non-selective Na+/H+ exchanger inhibitor--amiloride.</p><p><b>METHODS</b>Single ventricular cells were isolated using a double-enzyme method. Effects of amiloride on voltage-dependent potassium and calcium currents in isolated guinea pig ventricular myocyte were recorded by using whole-cell patch clamp techniques.</p><p><b>RESULTS</b>Exposure to amiloride (10 -100 micromol x L(-1)), the L-type and T-type calcium currents were depressed. Amiloride resulted in a concentration-dependent inhibition of peak (Ca,L), But amiloride did not change the shape of their I - V curves. It only decreased the amplitudes of the currents of the two types. When myocytes were incubated with 100 micromol x L(-1) amiloride, I(Kr) was slightly depressed and I(Ks) did not change. Amiloride (1 - 100 micromol x L(-10) depressed I(K1) in a concentration-dependent manner.</p><p><b>CONCLUSION</b>Amiloride depressed potassium and calcium currents, which may give support to its uses in some diseases of the cardiovascular system.</p>
Subject(s)
Animals , Female , Male , Amiloride , Pharmacology , Anti-Arrhythmia Agents , Pharmacology , Calcium Channels, L-Type , Calcium Channels, T-Type , Cell Separation , Guinea Pigs , Heart Ventricles , Cell Biology , Myocytes, Cardiac , Patch-Clamp Techniques , Potassium Channels, Inwardly Rectifying , Potassium Channels, Voltage-Gated , Sodium-Hydrogen ExchangersABSTRACT
<p><b>AIM</b>To investigate the effect of benzyltetrahydropalmatine (BTHP) on the rapidly activating component of delayed rectifier K+ current (Ikr) in single guinea pig ventricular myocytes.</p><p><b>METHODS</b>Whole-cell patch clamp technique was used to record Ikr.</p><p><b>RESULTS</b>Ikr was blocked by 1-100 mumol.L-1 BTHP in concentration-, voltage-, and specifically frequency-dependent fashion, with IC50 of 13.5 mumol.L-1 (95% confidence range: 11.2-15.8 mumol.L-1). 30 mumol.L-1 BTHP reduced Ikr and Ikr.tail by (31 +/- 4)% and (36 +/- 5)% (n = 6, P < 0.01), respectively. The time constant for deactivation (tau') of the tail current was decreased by 30 mumol.L-1 BTHP from (238 +/- 16) ms to (196 +/- 14) ms, while drug had no any effect on the time constant for activation (tau) of Ikr,tail.</p><p><b>CONCLUSION</b>BTHP inhibited Ikr in a frequency-dependent fashion.</p>