Effects of relaxin on rat atrial myocytes. i. inhibition of i to
via pka-dependent phosphorylation.
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 3:0498H, 1996.
The peptide hormone relaxin has direct, positive inotropic and
chronotropic effects on rat hearts in vivo and in vitro. Relaxin's
effects on the electrophysiological properties of single quiescent
atrial cells from normal rats was investigated using whole-cell
patch-clamp. Relaxin had a significant inhibitory effect on outward
potassium currents. Outward potassium currents consisted of a
transient component (Ito) and a sustained component (IS). Addition of
100 ng/ml of relaxin inhibited peak Ito in a voltage-dependent manner
(74% inhibition at Vm=-10 mV to 30% inhibition at +70 mV). The time
to reach peak Ito and the apparent time constant of inactivation of
Ito ([tau]decay) were increased by relaxin. Dialysis with 2 [mu] M of
the protein kinase A inhibitor 5-24 amide prevented relaxin's
effects, suggesting an obligatory role for this kinase in the
relaxin-dependent regulation of potassium current.
Received 3 June 1996; accepted in final form 30 October 1996.
APS Manuscript Number H497-6.
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