Endothelin-1 (10 nM) had opposite effects on the L-type Ca2+ current in human atrial myocytes, increasing low-density current by 99% and decreasing high-density current by 33%.
Does endothelin-1 alter the L-type Ca2+ current in human atrial myocytes?
Endothelin-1 has dual, baseline-dependent effects on L-type Ca2+ currents in human atrial myocytes, involving both ETA and ETB receptors.
The effects of endothelin-1 (ET-1) on the L-type Ca2+ current (I(Ca)) were examined in whole cell patch-clamped human atrial myocytes. Depending on the initial current density, ET-1 (10 nM) increased the amplitude of I(Ca) 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 I(Ca) of higher density (5.8 +/- 0.3 pA/pF) was inhibited by ET-1. After I(Ca) stimulation by 1 microM 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 I(Ca) (41 +/- 3%) by reducing intracellular cAMP concentration. In ANP-treated myocytes, the stimulatory effect of ET-1 on I(Ca) predominated (52 +/- 7%). The inhibitory effect of ET-1 on I(Ca) was blocked by the ET(A) antagonist BQ-123, whereas the stimulatory effect was suppressed by the ET(B) agonist BQ-788. We conclude that ET-1 has opposite effects on I(Ca) depending on the baseline amplitude of current, and both subtype ET receptors are implicated in the signal transduction pathways.
Boixel et al. (Wed,) conducted a other in Human atrial myocytes. Endothelin-1 (ET-1) vs. Baseline current was evaluated on L-type Ca2+ current (I(Ca)) amplitude. Endothelin-1 (10 nM) had opposite effects on the L-type Ca2+ current in human atrial myocytes, increasing low-density current by 99% and decreasing high-density current by 33%.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: