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Intracellular calcium during excitation in mammalian heart muscle
J Mol
,14
Cell
Cardiol20
(Supplement
IV) (1988)
INTRACELLULAR CALCIUM DURING EXCITATION IN MAMMALIAN HEART MUSCLE. W. J. Lederer, Dept. Physiology, Univ. Maryland Sch. Medicine, M.B. Cannel1 C J.R. Berlin. Baltimore, MD 21201, USA; Dept. Pharmacology, Univ. Miami Med. School, Miami, FL, USA. We have examined the mechanisms that control intracellular calcium, [Ca*+], in rat heart muscle during and following electrical excitation. Using furaand indo-l loaded dissociated sin le cells under voltage-clamp control, we examined the voltagedependence of the [Ca 2$ ]i transient and of the calcium current, 1~~. We have observed 5 important features. (1). We find that the half-maximal voltage activating the [Ca*+] transient is about 12 mV more negative than the half-maximal voltage activating (2). We find that brief (less than 50 msec) depolarizations are associated with %a. smaller calcium transients. (3). Very positive depolarizations (i.e. positive to + 50 mV) may lead to a secondary calcium transient on repolarization. (4). No calcium transients are observed during depolarization to extremely positive (i.e. +lOO mV) but -'repolarization transients" are seen following the depolarization. (5) An Ica tail current accompanies the repolarization [Ca2+]-transient. Ryanodine (25 uM) blocks SO-90% of the calcium transient. These results suggest that neither a simple calciuminduced calcium release mechanism nor a simple voltage-dependent calcium-release Additionally, the mechanism control excitation-contraction coupling in rat heart. results suggest that a voltage-activated Na-Ca exchange mechanism does NOT carry calcium into the cell to activate a calcium-induced calcium release mechanism.
s.22
,14
Cell
Cardiol20
(Supplement
IV) (1988)
INTRACELLULAR CALCIUM DURING EXCITATION IN MAMMALIAN HEART MUSCLE. W. J. Lederer, Dept. Physiology, Univ. Maryland Sch. Medicine, M.B. Cannel1 C J.R. Berlin. Baltimore, MD 21201, USA; Dept. Pharmacology, Univ. Miami Med. School, Miami, FL, USA. We have examined the mechanisms that control intracellular calcium, [Ca*+], in rat heart muscle during and following electrical excitation. Using furaand indo-l loaded dissociated sin le cells under voltage-clamp control, we examined the voltagedependence of the [Ca 2$ ]i transient and of the calcium current, 1~~. We have observed 5 important features. (1). We find that the half-maximal voltage activating the [Ca*+] transient is about 12 mV more negative than the half-maximal voltage activating (2). We find that brief (less than 50 msec) depolarizations are associated with %a. smaller calcium transients. (3). Very positive depolarizations (i.e. positive to + 50 mV) may lead to a secondary calcium transient on repolarization. (4). No calcium transients are observed during depolarization to extremely positive (i.e. +lOO mV) but -'repolarization transients" are seen following the depolarization. (5) An Ica tail current accompanies the repolarization [Ca2+]-transient. Ryanodine (25 uM) blocks SO-90% of the calcium transient. These results suggest that neither a simple calciuminduced calcium release mechanism nor a simple voltage-dependent calcium-release Additionally, the mechanism control excitation-contraction coupling in rat heart. results suggest that a voltage-activated Na-Ca exchange mechanism does NOT carry calcium into the cell to activate a calcium-induced calcium release mechanism.
s.22