Calmodulin kinase II accelerates L-type Ca2+ current recovery from inactivation and compensates for the direct inhibitory effect of [Ca2+]i in rat ventricular myocytes.

The Journal of Physiology
Jiqing Guo, H J Duff

Abstract

Some studies report that the positive relationship between L-type Ca(2+) current (I(Ca-L)) and frequency in cardiac myocytes is mainly due to a direct negative feedback of sarcoplasmic reticulum Ca(2+) release on I(Ca-L) inactivation while others provide evidence for activation of calmodulin kinase II (CaMKII). To further elucidate the role of endogenous CaMKII activity, the CaMKII inhibitory peptides, autocamtide-2 relating inhibitory peptide (AIP) and myristoylated AIP were applied using conventional and perforated patch-clamp methods. AIP inhibited the normal adaptive increase in I(Ca-L) in response to abrupt increase in pacing frequency from 0.05 to 2 Hz. The positive I(Ca-L)-frequency relationship was reversed by AIP and the inhibitory effect of AIP was significantly exaggerated at fast pacing rates. The onset of inactivation of I(Ca-L) was not altered by AIP. After thapsigargin treatment, AIP slowed recovery from inactivation of I(Ca-L) and this effect was exaggerated during fast pacing. Buffering of [Ca(2+)](i) by BAPTA and EGTA accelerated recovery of I(Ca-L) from inactivation, and BAPTA partly eliminated the effect of AIP on the recovery. We conclude that: (1) [Ca(2+)](i) directly slows I(Ca-L) recovery from inactivati...Continue Reading

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Citations

May 19, 2010·Proceedings of the National Academy of Sciences of the United States of America·Anne BlaichSven Moosmang
Apr 1, 2009·Journal of Cardiovascular Pharmacology·Donald M Bers, Eleonora Grandi
Oct 25, 2011·American Journal of Physiology. Heart and Circulatory Physiology·Hendrick E D J ter Keurs
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Sep 29, 2020·The Journal of General Physiology·Alejandra Cely-OrtizAlicia Mattiazzi
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