Please use this identifier to cite or link to this item:
https://elar.urfu.ru/handle/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://elar.urfu.ru/handle/10995/101385 |
Access: | info:eu-repo/semantics/openAccess |
SCOPUS ID: | 85092750530 |
WOS ID: | 000582938000017 |
PURE ID: | 5d7b0bd3-972e-412c-9091-b9f1c778a64b 14159752 |
ISSN: | 220949 |
DOI: | 10.1242/jeb.228205 |
Sponsorship: | The study was supported by the Russian Foundation for Basic Research (19-34-90142 to D.V.A.). |
Appears in Collections: | Научные публикации ученых УрФУ, проиндексированные в SCOPUS и WoS CC |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
2-s2.0-85092750530.pdf | 972,37 kB | Adobe PDF | View/Open |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.