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Discordant interventricular differences in the excitation‐contraction coupling explained by the lower levels of troponin and Ca 2+ buffering in the right ventricle of rats
Author(s) -
Jeon Young Keul,
Kwon Jae Won,
Kim Sung Joon
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.03266
Subject(s) - ventricle , medicine , chemistry , contractility , contraction (grammar) , interventricular septum , biophysics , troponin c , troponin , calcium , cardiology , biology , myocardial infarction
The left and right ventricles have distinctive functional characteristics as well as the anatomical differences. However, precise understanding of interventricular differences in the excitation‐contraction (E‐C) coupling mechanisms and the Ca 2+ homeostasis is still lacking. Here we compared the results from the right and left cardiomyocytes (RVCMs and LVCMs) of rats by using whole‐cell patch clamp and IonOptix measuring cytosolic Ca 2+ ([Ca 2+ ] i ) and contractility. RVCMs showed significantly shorter action potential duration (APD), with higher density of transient outward K + current ( I to ) while similar L‐type Ca 2+ current. However, the triggered [Ca 2+ ] i change (Ca 2+ transient) was not different while the decaying rate of Ca 2+ transient was slower in RVCMs. More perplexingly, the sarcomere shortening amplitude (DSL) was smaller and the relaxation speed was slower in RVCMs than LVCMs. The analysis of SERCA activity in situ revealed approximately 50% lower level in RVCMs. Interestingly, the immunoblot analysis revealed lower expression of cardiac troponin complex (cTnC, cTnI and cTnT) in RVCMs. The lower Ca 2+ binding cTnC implied smaller Ca 2+ buffering capacity ( κ S ), which could be responsible for the similar amplitude of Ca 2+ ‐transient despite the shorter APD in RVCMs. In situ analysis using known concentration of fura‐2 revealed lower κ S in the RVCMs. Introduction of the 1.9 fold I to , 0.5 fold SERCA, and 0.7 fold cTn into the mathematical model of rat LVCM reproduced the similar Ca 2+ transient and the slower Ca 2+ decay along with the shorter APD of RVCM. Taken together, we firstly show the lower expression of cTn proteins in the RVCMs, which gives a clue to explain the inter‐ventricular difference in the E‐C coupling kinetics.