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1 Institut National de la Santé et de la Recherche Médicale U460, Faculté de Médecine Xavier Bichat, 75018 Paris; 2 Service de Cardiologie Hôpital Antoine Béclère, 92141 Clamart; and 3 Service de Chirurgie Cardiaque and 4 Service de Physiologie-Explorations Fonctionnelles, Groupe Hospitalier Bichat-Claude Bernard, Assistance Publique-Höpitaux de Paris, 75018 Paris, France
The effects of endothelin-1 (ET-1) on the L-type Ca2+ current (ICa) were examined in whole cell patch-clamped human atrial myocytes. Depending on the initial current density, ET-1 (10 nM) increased the amplitude of ICa by 99 ± 7% or decreased it by 33 ± 2%. The stimulatory effect predominated on current of low density (2.3 ± 0.2 pA/pF), whereas ICa of higher density (5.8 ± 0.3 pA/pF) was inhibited by ET-1. After ICa stimulation by 1 µM isoproterenol, ET-1 always inhibited the current by 32 ± 7% (P < 0.05), an effect that was suppressed by pretreating myocytes with pertussis toxin. Atrial natriuretic peptide (ANP) inhibited ICa (41 ± 3%) by reducing intracellular cAMP concentration. In ANP-treated myocytes, the stimulatory effect of ET-1 on ICa predominated (52 ± 7%). The inhibitory effect of ET-1 on ICa was blocked by the ETA antagonist BQ-123, whereas the stimulatory effect was suppressed by the ETB agonist BQ-788. We conclude that ET-1 has opposite effects on ICa depending on the baseline amplitude of current, and both subtype ET receptors are implicated in the signal transduction pathways.
human cardiac cells; whole cell patch clamp
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