Changes in myoplasmic Ca2+ during fatigue differ between FDB fibers, between glibenclamide-exposed and Kir6.2-/- fibers and are further modulated by verapamil

Physiological Reports
David Selvin, Jean-Marc Renaud

Abstract

One objective of this study was to document how individual FDB muscle fibers depend on the myoprotection of KATP channels during fatigue. Verapamil, a CaV1.1 channel blocker, prevents large increases in unstimulated force during fatigue in KATP-channel-deficient muscles. A second objective was to determine if verapamil reduces unstimulated [Ca(2+)]i in KATP-channel-deficient fibers. We measured changes in myoplasmic [Ca(2+)] ([Ca(2+)]i) using two KATP-channel-deficient models: (1) a pharmacological approach exposing fibers to glibenclamide, a channel blocker, and (2) a genetic approach using fibers from null mice for the Kir6.2 gene. Fatigue was elicited with one tetanic contraction every sec for 3 min. For all conditions, large differences in fatigue kinetics were observed from fibers which had greater tetanic [Ca(2+)]i at the end than at the beginning of fatigue to fibers which eventually completely failed to release Ca(2+) upon stimulation. Compared to control conditions, KATP-channel-deficient fibers had a greater proportion of fiber with large decreases in tetanic [Ca(2+)]i, fade and complete failure to release Ca(2+) upon stimulation. There was, however, a group of KATP-channel-deficient fibers that had similar fatigue ki...Continue Reading

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Citations

Jan 6, 2017·Journal of Bioenergetics and Biomembranes·E Sánchez-DuarteR Montoya-Pérez

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