Barium- and calcium-permeable channels open at negative membrane potentials in rat ventricular myocytes

Coulombe, Alain; Lefevre, Isabel A.; Baró, Isabelle; Coraboeuf, E

doi:10.1007/bf01869209

Cited by 52 publications

(31 citation statements)

References 30 publications

(33 reference statements)

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“…T-type channels are present in some, but not all, species [16,22] but their role in regulating resting [Ca 2+ ] i is not known. Background channels have been reported [10,21] and may contribute. The existence of Na + -independent mechanisms for Ca 2+ influx is shown by the fact that, even in the absence of Na + ions, elevating external [Ca 2+ ] increases [Ca 2+ ] i [19].…”

Section: Introductionmentioning

confidence: 95%

Measurement of calcium entry and exit in quiescent rat ventricular myocytes

Choi

Trafford

Eisner

2000

Pflugers Arch - Eur J Physiol

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The aim of this work was to obtain the first quantitative measurements of Ca2+ influx and efflux in quiescent cardiac cells. The relationship between free and total Ca2+ was obtained during a caffeine application. This buffering curve was then used to calculate changes of total Ca2+ from measurements of free cytosolic [Ca2+] ([Ca2+]i) made with Indo-1. The rate of Ca2+ removal from the cytoplasm was calculated by differentiating total Ca2+ with respect to time. The dependence of d(total Ca2+)/dt on [Ca2+]i was hyperbolic. Inhibition of either Na+-Ca2+ exchange (by addition of 10 mmol l(-1) NiCl2 or removal of external Na+) or the sarcolemmal Ca2+-activated adenosine triphosphatase (Ca2+-ATPase) (with carboxyeosin) decreased the calculated efflux. In both cases, the main effect was on the apparent maximum rate (Vmax) with little effect on the Michaelis-Menten constant (Km). These results suggest that the Na+-Ca2+ exchange and Ca2+-ATPase have very similar affinities for [Ca2+]i and that their fractional contributions do not change over the systolic range of [Ca2+]i. Ca2+ influx was quantified in two ways. The first method was to extrapolate the curve relating Ca2+ efflux to [Ca2+]i to zero [Ca2+]i. This gave a value of 4.49+/-0.54 micromol l(-1) s(-1) which was reduced to zero by either removal of external Ca2+ or addition of Ni2+. In other experiments external Ca2+ was removed and the maximum rate of fall of total Ca2+ calculated as 2.53+/-0.93 micromol l(-1) s(-1). This approach can be used to provide a quantitative analysis of the control of resting [Ca2+]i.

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Section: Introductionmentioning

confidence: 95%

Measurement of calcium entry and exit in quiescent rat ventricular myocytes

Choi

Trafford

Eisner

2000

Pflugers Arch - Eur J Physiol

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“…Under resting conditions with a normal resting membrane potential, voltage gated L-and T-type calcium channels would not be expected to be open [15]; however, there is evidence for the presence of background calcium channels (B-type) in rat ventricular myocytes even at negative membrane potentials [6,11] They are relatively abundant [6] compared with the paucity of voltage-activated channels [13]. It is possible therefore that the rise in [Ca2+] ; observed in the absence of extracellular sodium is via these B-type calcium channels and that a proportion of the calcium entering the muscle in the presence of extracellular sodium enters by this route.…”

Section: Calcium Extrusion By Sarcolemmal Mechanismsmentioning

confidence: 99%

The sarcolemmal mechanisms involved in the control of diastolic intracellular calcium in isolated rat cardiac trabeculae

Lamont

Eisner

1996

Pflügers Arch — Eur J Physiol

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We performed experiments using the calcium indicator Indo-1 to determine the relative roles of the sarcolemmal mechanisms involved in the regulation of diastolic intracellular calcium concentration ([Ca2+]i) in trabeculae from the rat heart. Ryanodine was used to eliminate sarcoplasmic reticulum (SR) function. In the functional absence of the SR, 76.8 +/- 3.9% of the calcium was extruded by the Na-Ca exchange carrier in the [Ca2+]i range of diastolic concentration +/- 200-400 nM. This was assessed by measuring the recovery of [Ca2+]i from small perturbations in the presence and absence of extracellular sodium. The steady-state relationship between [Ca2+]o and [Ca2+]i was linear over the range of 1-40 mM, a 20-fold increase of [Ca2+]o produced a 1.97-fold +/- 0.13-fold increase in [Ca2+]i (n = 5). In the absence of extracellular sodium raising [Ca2+]o had a variable effect. In some preparations there was little change of [Ca2+]i while in others the response was almost as large as in control conditions. We conclude that the Na-Ca exchanger contributes approximately 77% of sarcolemmal calcium extrusion following small perturbations in [Ca2+]i and that this fraction does not diminish as the [Ca2+]i declines. In addition we have shown a sodium-independent entry of calcium into quiescent cardiac muscle under resting conditions.

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“…This channel showed a significant permeability to divalent cations but not to monovalent cations such as K ＋ and Na ＋ ions [35].…”

Section: Background Ca 2＋ Leak Current (Icab)mentioning

confidence: 98%

“…Ca 2＋ leak or background Ca 2＋ channel has been reported in adult rat ventricular myocytes [35,36]. This channel showed a significant permeability to divalent cations but not to monovalent cations such as K ＋ and Na ＋ ions [35].…”

Section: Background Ca 2＋ Leak Current (Icab)mentioning

confidence: 99%

A Computational Model of Cytosolic and Mitochondrial [Ca2+] in Paced Rat Ventricular Myocytes

Youm

Choi

Jang

et al. 2011

Korean J Physiol Pharmacol

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INTRODUCTIONThe major role of ventricular myocardium is to contract regularly in response to electrical excitation in order to pump oxygenated blood out of ventricle. Two key elements are directly involved in the normal cycle of contractile activity in ventricular myocytes. One is intracellular Ca 2＋ -cycling and the other is ATP synthesis by mitochondria. Upon release from sarcoplasmic reticulum (SR), Ca 2＋ binds to troponin C to move the tropomyosin away exposing the myosin-binding site of actin filament. If ATP and Ca 2＋ are high enough near the contractile apparatus, the cross bridge cycle continues and muscle would contract. In the end of contraction, majority of Ca 2＋ is pumped back into the Ca 2＋ store by SR Ca 2＋ pump then muscle relaxes.Therefore, disruption of either Ca 2＋-cycling or ATP synthesis can disturb normal cycle of ventricular contraction. ATP synthesis by mitochondria can directly or indirectly affect the Ca 2＋ -cycling by regulating the ATP-driven SR Ca 2＋ pump [1,2] and sarcolemmal Na ＋ /K ＋ pump [1].Metabolic inhibitors are supposed to suppress the normal cycle of contraction via this mechanism. There has been evidence that Ca 2＋-cycling affects the ATP synthesis in mitochondria. Increased mitochondrial Ca 2＋ influx across the inner mitochondrial membrane has been known to stimulate F0F1-ATPase activity [3,4]. Increase in mitochondrial [Ca 2＋ ] ([Ca 2＋ ]m) has also been known to stimulate tricarboxylic acid (TCA) cycle dehydrogenases [5,6]. The resultant increase in NADH could affect the ATP synthesis of mitochondria. This is supposed to be the control mechanism that matches energy demand for bigger contraction induced by higher cytosolic (or intracellular) [Ca 2＋ ] ( [Ca 2＋ ]i) [7]. There is a controversial issue on the possibility that [Ca 2＋ ]m changes in a beat-to-beat manner. Beat-to-beat mitochondrial Ca 2＋ transients have been identified on adult 218JB Youm, et al rabbit cardiac myocytes [8] and on rat cardiac myocytes [9]. In contrast, beat-to-beat change in [Ca 2＋ ]m was not identified on cat ventricular myocytes [10]. Further complicating thing is that the ATP depletion can affect action potential (AP) waveform by stimulating ATP sensitive K ＋ channel.Reduced action potential duration (APD) by activation of ATP sensitive K ＋ channel can reduce the energy demand during contraction. All above observations demonstrate how complex the interaction among Ca 2＋-cycling, ATP production, and electrical excitation could be. If all those elements are properly modeled, an integrated mathematical model could be developed and utilized to investigate those complex interactions.Recently, cardiac models integrating electrophysiology, Ca 2＋ cycling, and energy metabolism have emerged based on experimental results from guinea pig ventricular myocytes [11,12]. Although they were able to couple mitochondrial energetics to excitation-contraction coupling, the description of mitochondrial ion transport is limited and the modeling of pHm and pHi is lacking which is a key elem...

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Barium- and calcium-permeable channels open at negative membrane potentials in rat ventricular myocytes

Cited by 52 publications

References 30 publications

Measurement of calcium entry and exit in quiescent rat ventricular myocytes

Measurement of calcium entry and exit in quiescent rat ventricular myocytes

The sarcolemmal mechanisms involved in the control of diastolic intracellular calcium in isolated rat cardiac trabeculae

A Computational Model of Cytosolic and Mitochondrial [Ca2+] in Paced Rat Ventricular Myocytes

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