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1.
Acta Pharmaceutica Sinica ; (12): 509-513, 2004.
Article Dans Anglais | WPRIM | ID: wpr-302775

Résumé

<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>


Sujets)
Animaux , Femelle , Mâle , Amiloride , Pharmacologie , Antiarythmiques , Pharmacologie , Canaux calciques de type L , Canaux calciques de type T , Séparation cellulaire , Cochons d'Inde , Ventricules cardiaques , Biologie cellulaire , Myocytes cardiaques , Techniques de patch-clamp , Canaux potassiques rectifiants entrants , Canaux potassiques voltage-dépendants , Antiport des ions sodium-hydrogène
2.
Acta Pharmaceutica Sinica ; (12): 603-607, 2002.
Article Dans Anglais | WPRIM | ID: wpr-312072

Résumé

<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>


Sujets)
Animaux , Femelle , Mâle , Antiarythmiques , Pharmacologie , Alcaloïdes de type berbérine , Pharmacologie , Séparation cellulaire , Canaux potassiques rectifiants retardés , Cochons d'Inde , Ventricules cardiaques , Biologie cellulaire , Métabolisme , Myocytes cardiaques , Métabolisme , Techniques de patch-clamp , Canaux potassiques , Métabolisme , Canaux potassiques voltage-dépendants
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