Please use this identifier to cite or link to this item: http://hdl.handle.net/10995/101385
Title: Warmer, faster, stronger: Ca2+ cycling in avian myocardium
Authors: Filatova, T. S.
Abramochkin, D. V.
Shiels, H. A.
Issue Date: 2020
Publisher: Company of Biologists Ltd
Citation: Filatova T. S. Warmer, faster, stronger: Ca2+ cycling in avian myocardium / T. S. Filatova, D. V. Abramochkin, H. A. Shiels. — DOI 10.1242/jeb.228205 // Journal of Experimental Biology. — 2020. — Vol. 223. — Iss. 19. — jeb228205.
Abstract: Birds occupy a unique position in the evolution of cardiac design. Their hearts are capable of cardiac performance on par with, or exceeding that of mammals, and yet the structure of their cardiomyocytes resembles those of reptiles. It has been suggested that birds use intracellular Ca2+ stored within the sarcoplasmic reticulum (SR) to power contractile function, but neither SR Ca2+ content nor the cross-talk between channels underlying Ca2+-induced Ca2+ release (CICR) have been studied in adult birds. Here we used voltage clamp to investigate the Ca2+ storage and refilling capacities of the SR and the degree of trans-sarcolemmal and intracellular Ca2+ channel interplay in freshly isolated atrial and ventricular myocytes from the heart of the Japanese quail (Coturnix japonica). A trans-sarcolemmal Ca2+ current (ICa) was detectable in both quail atrial and ventricular myocytes, and was mediated only by L-type Ca2+ channels. The peak density of ICa was larger in ventricular cells than in atrial cells, and exceeded that reported for mammalian myocardium recorded under similar conditions. Steadystate SR Ca2+ content of quail myocardium was also larger than that reported for mammals, and reached 750.6±128.2 μmol lâ'1 in atrial cells and 423.3±47.2 μmol lâ'1 in ventricular cells at 24°C. We observed SR Ca2+-dependent inactivation of ICa in ventricular myocytes, indicating cross-talk between sarcolemmal Ca2+ channels and ryanodine receptors in the SR. However, this phenomenon was not observed in atrial myocytes. Taken together, these findings help to explain the high-efficiency avian myocyte excitation-contraction coupling with regard to their reptilian-like cellular ultrastructure. © 2020 Company of Biologists Ltd. All rights reserved.
Keywords: BIRD
COTURNIX JAPONICA
EXCITATION-CONTRACTION COUPLING
HEART
L-TYPE CA2+ CURRENT
SARCOPLASMIC RETICULUM
CALCIUM
RYANODINE RECEPTOR
ANIMAL
CARDIAC MUSCLE
CARDIAC MUSCLE CELL
COTURNIX
HEART CONTRACTION
HEART VENTRICLE
METABOLISM
SARCOPLASMIC RETICULUM
ANIMALS
CALCIUM
COTURNIX
HEART VENTRICLES
MYOCARDIAL CONTRACTION
MYOCARDIUM
MYOCYTES, CARDIAC
RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL
SARCOPLASMIC RETICULUM
URI: http://hdl.handle.net/10995/101385
Access: info:eu-repo/semantics/openAccess
SCOPUS ID: 85092750530
PURE ID: 14159752
5d7b0bd3-972e-412c-9091-b9f1c778a64b
ISSN: 220949
DOI: 10.1242/jeb.228205
metadata.dc.description.sponsorship: The study was supported by the Russian Foundation for Basic Research (19-34-90142 to D.V.A.).
Appears in Collections:Научные публикации, проиндексированные в SCOPUS и WoS CC

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