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Cardiovascular Research 1999 44(1):146-155; doi:10.1016/S0008-6363(99)00200-X
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Abnormal Ca2+ release from cardiac sarcoplasmic reticulum in tachycardia-induced heart failure

Takeshi Yamamoto, Masafumi Yano*, Michihiro Kohno, Takayuki Hisaoka, Kaoru Ono, Taketo Tanigawa, Yukio Saiki, Yuhji Hisamatsu, Tomoko Ohkusa and Masunori Matsuzaki

Second Department of Internal Medicine, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan

* Corresponding author. +81-836-22-2248; fax: +81-836-22-2246

Objective: In heart failure, little information is available as to the Ca2+ release function of sarcoplasmic reticulum (SR), which plays a major role in cardiac contractile function. Here, we assessed the rapid kinetics of drug-induced Ca2+ release from cardiac SR in combination with a measurement of ryanodine binding in heart failure. Methods: The SR vesicles were isolated from dog left ventricular (LV) muscles (normal (N), n=10; pacing induced heart failure (HF), n=10). The time course of SR Ca2+ release was continuously monitored by a stopped-flow apparatus using arsenazoIII as a Ca2+ indicator, and Ca2+ uptake and [3H]ryanodine binding assays were done using a filtration method. Results: The amount of Ca2+ uptake was reduced in HF to 55% of N (P<0.05). Even the more marked and earlier appeared decrease was seen in the rate constant and the initial rate of polylysine (PL; a specific release trigger)-induced Ca2+ release (P<0.05). However, the PL concentration dependency of the initial rate shifted towards lower concentrations of PL in HF than in N ([PL] at half maximum stimulation=0.13 vs. 0.35 µM). The [3H]ryanodine binding assay revealed a lower Bmax (pmol/mg) in HF than in N (0.91±0.19 vs. 2.64±0.59, P<0.05), but no difference in Kd (nM) (0.95±0.29 vs. 0.90±0.11, P=n.s.). The [PL] dependency on the enhancement of [3H]ryanodine binding again showed a shift towards lower [PL] in HF than in N. Conclusions: In pacing-induced heart failure, the Ca2+ releasing function of SR is disturbed, which may result in an intra-cellular Ca2+ transient that was slowed down.

KEYWORDS SR, sarcoplasmic reticulum; E–C coupling, excitation–contraction coupling; PMSF, phenylmethanesulfonyl fluoride; MES, 2-(N-morpholino)ethanesulfonic acid; MOPS, 3-[N-morpholino]propanesulfonic acid; EGTA, ethylene glycol bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid


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