Properties of transmembrane ca2+ current at physiologic
temperatures relevant to the action potential in human atrial
myocytes.
Li, Gui-Rong, and Stanley Nattel.
Department of Medicine and Research Center, Montreal Heart
Institute and University of Montreal, Department of Pharmacology and
Therapeutics, McGill University, Montreal, Quebec H1T 1C8, Canada
APStracts 3:0356H, 1996.
There are no published characterizations of ICa at physiologic
temperatures in human atrium. Depolarization of human atrial myocytes
at 36 degrees C elicited ICa which peaked at +10 mV, with a mean
maximum current density of 10.8 +/- 1.1 pA/pF and no evidence for T
-type current. Overlap between activation and inactivation curves and
incomplete inactivation during pulses comparable to normal action
potential duration (APD) were compatible with the observed role of
ICa in maintaining the plateau. ICa was frequency-dependent between
0.1 and 2 Hz, and ICa blockade with 0.2 mM Cd2+ reduced rate
-dependent changes in APD: under control, APD at 90% repolarization
was 230 +/- 15 ms at 0.1 Hz and 178 +/- 14 ms at 2 Hz (decrease of 52
+/- 5 ms); with Cd2+, values were 121 +/- 7 ms at 0.1 Hz and 115 +/-
6 ms at 2 Hz (decrease of 6?+/-?3 ms, P < 0.01). Isoproterenol
(1 [mu]M) increased ICa and prolonged APD from 138 +/- 13 to 199 +/-
15 ms (P < 0.01). These results indicate that, in human atrial
cells at 36oC, the properties of L-type ICa contribute importantly to
the rate-dependent and autonomic control of APD.
Received 29 March 1996; accepted in final form 1 August 1996.
APS Manuscript Number H299-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996