β3-Adrenergic Regulation of L-Type Ca2+ Current and Force of Contraction in Human Ventricle

β3-Adrenergic Regulation of L-Type Ca2+ Current and Force of Contraction in Human Ventricle β3-Adrenergic receptor (β3-AR) is expressed in human atrial and ventricular tissues. Recently, we have demonstrated that it was involved in the activation of L-type Ca2+ current (I Ca,L) in human atrial myocytes and the force of contraction of human atrial trabeculae. In the present study, we examined the effect of β3-AR agonist CGP12177 which also is a β1-AR/β2-AR antagonist on I Ca,L in human ventricular myocytes (HVMs) and the force of contraction of human ventricular trabeculae. CGP12177 stimulated I Ca,L in HVMs with high potency but much lower efficacy than isoprenaline. The β3-AR antagonist L-748,337 inhibited the effect of CGP12177. CGP12177 and L748,337 competed selectively on β3-ARs because L748,337 had no effect on isoprenaline-induced stimulation of I Ca,L, while CGP12177 completely blocked the effect of isoprenaline. The activation of β3-ARs by CGP12177 does not involve the activation of Gi proteins because CGP12177 had no effect on forskolin-induced stimulation of I Ca,L. CGP12177 had no effect on the force of contraction of human ventricular trabeculae. L-NMMA, an inhibitor of NO synthase, and IBMX, a nonselective inhibitor of phosphodiesterases, did not potentiate the effect of CGP12177 either on contraction of human ventricular trabeculae or on I Ca,L in HVMs. We conclude that in human ventricles β3-AR activation has no inotropic effect, while it slightly increases I Ca,L. In contrast to human atrium, the activation of β3-ARs in human ventricle is not accompanied by increased activity of phosphodiesterases. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

β3-Adrenergic Regulation of L-Type Ca2+ Current and Force of Contraction in Human Ventricle

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Publisher
Springer US
Copyright
Copyright © 2014 by Springer Science+Business Media New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-014-9635-2
Publisher site
See Article on Publisher Site

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