Effects of relaxin on rat atrial myocytes. ii. increased calcium
influx derived from action potential prolongation.
Piedras-Renter[acute]ia, Erika S., O. David Sherwood and Philip M.
Best
Department of Molecular and Integrative Physiology and School of
Medicine, University of Illinois at Urbana-Champaign, Urbana, IL
61801
APStracts 3:0499H, 1996.
Relaxin produces positive inotropic and chronotropic effects in rat
hearts. The effect of relaxin on the action potential duration (APD)
of single quiescent rat atrial cells was investigated using whole
-cell patch clamp. Relaxin induced a significant, dose-dependent
prolongation of the APD. This effect was maximal at 200 ng/ml
(nominal concentration of 33.6 nM), which caused, on average, a 57%
increase in the time taken to reach 90% repolarization. The effect of
relaxin was blocked by the PKA inhibitor 5-24 amide, indicating that
its effect is mediated by a cAMP-dependent mechanism. The increased
APD induced by relaxin caused an enhanced entrance of calcium, with
the charge carried through voltage activated calcium channels
increased by 25%. This increase was not due to a direct modulation of
calcium currents (20); rather, it was a consequence of the longer
period of cellular depolarization. Our findings that relaxin
increases the APD and therefore increased calcium influx in atrial
myocytes could explain the positive inotropic effects induced by
relaxin in atrial preparations.
Received 3 June 1996; accepted in final form 30 October 1996.
APS Manuscript Number H498-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996