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Title:Effects of relaxin on the electrophysiological properties of isolated atrial myocytes
Author(s):Piedras-Renteria, Erika Sofia
Doctoral Committee Chair(s):Best, Philip M.
Department / Program:Molecular and Integrative Physiology
Discipline:Physiology
Degree Granting Institution:University of Illinois at Urbana-Champaign
Degree:Ph.D.
Genre:Dissertation
Subject(s):Biology, Animal Physiology
Abstract:The reproductive hormone relaxin has direct, positive inotropic and chronotropic effects on rat atrial muscle both in vivo and in vitro. The effect of relaxin on the electrophysiological properties of single quiescent atrial cells from normal rats was investigated using whole-cell current-clamp and voltage-clamp techniques. Three major findings are presented: (1) Two components of outward potassium current were identified in atrial myocytes: a transient component (I$\rm\sb{to})$ and a sustained component $\rm(I\sb{S}).$ The transient outward potassium current was inhibited by relaxin. Addition of 100 ng/ml of relaxin inhibited peak I$\rm\sb{to}$ in a voltage-dependent manner (30 to 74%). The kinetics of activation (time to peak) and inactivation $\rm(T\sb{decay})$ of I$\rm\sb{to}$ were also modified (increased). Finally, the voltage dependency of steady state activation parameters V$\sb{50}$ and k were changed in the presence of relaxin. All these effects were prevented by inclusion of 2 $\mu$M of the PKA inhibitor 5-24 amide in the intracellular solution, indicating that its effect is mediated by a cAMP-dependent mechanism. (2) Relaxin induced a significant, dose-dependent prolongation of action potential duration. The effect of relaxin on the action potential 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 protein kinase A inhibitor 5-24 amide, suggesting that the elongation of the AP is induced by the inhibition of I$\rm\sb{to}.$ (3) Increased action potential duration induced by relaxin caused an enhanced movement of calcium through voltage-activated calcium channels. Total charge moved increased by $\sim$25%. This increase was not due to a direct modulation of L- or T-type calcium currents, it was rather a consequence of the longer period of cellular depolarization.
In summary, the ability of relaxin to decrease atrial outward potassium currents may account for the capability of the hormone to prolong the atrial action potential. This prolongation has been shown to cause an increased calcium influx that could ultimately account for the inotropic effects of the hormone observed in atrial tissue.
Issue Date:1996
Type:Text
Language:English
URI:http://hdl.handle.net/2142/21905
ISBN:9780591200355
Rights Information:Copyright 1996 Piedras-Renteria, Erika Sofia
Date Available in IDEALS:2011-05-07
Identifier in Online Catalog:AAI9712406
OCLC Identifier:(UMI)AAI9712406


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