Caffeine stimulates the reverse mode of Na+/Ca2+ exchanger in ferret ventricular muscle

Léoty, Claude; Huchet-Cadiou, C.; Talon, Sophie; Choisy, Stéphanie C.M.; Hleihel, Walid

doi:10.1046/j.1365-201x.2001.00819.x

Cited by 6 publications

(4 citation statements)

References 22 publications

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“…This further suggests that ER-dependent Ca 2+ release has a minor contribution in the mitochondria-mediated toxicity of G93A. The rate of increase in Fura-2 fluorescence following caffeine application was slower and did not resume the baseline, which is likely due to the slow activity of the mitochondrial Na + /Ca 2+ exchanger, the major pathway for mitochondrial Ca 2+ efflux [ 75 ]. Observations of different pharmacological conditions support the concept that the presence of G93A severely disrupts mitochondrial Ca 2+ regulation.…”

Section: Discussionmentioning

confidence: 99%

Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease

et al. 2009

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Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons (MN) in the brain stem and spinal cord. Intracellular disruptions of cytosolic and mitochondrial calcium have been associated with selective MN degeneration, but the underlying mechanisms are not well understood. The present evidence supports a hypothesis that mitochondria are a target of mutant SOD1-mediated toxicity in familial amyotrophic lateral sclerosis (fALS) and intracellular alterations of cytosolic and mitochondrial calcium might aggravate the course of this neurodegenerative disease. In this study, we used a fluorescence charged cool device (CCD) imaging system to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells in an established cellular model of ALS.

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Section: Discussionmentioning

confidence: 99%

Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease

et al. 2009

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“…However, analysis of the actions of caffeine is complicated because of its multiplicity of actions in cardiac muscle. Although caffeine increases the rate of activator Ca 2+ from the SR and inhibits post-rest stimulation in mammals (Siegl, 1986), studies have also indicated that caffeine can modulate Ca 2+ sensitivity of contractile proteins (Wendt and Stephenson, 1983), increase activator Ca 2+ through inhibition of phosphodiesterase and subsequent increase flux through the sarcolemma (Siegl, 1986), decrease Ca 2+ -ATPase activity (Gupta et al, 1990) and even stimulate the reverse mode of the Na + /Ca 2+ exchanger (Léoty et al, 2001). While the present experiments of caffeine-induced contraction provide further evidence that sex differences exist in Ca 2+ handling by trout cardiac tissue, the exact mechanism remains to be elucidated.…”

Section: +mentioning

confidence: 99%

Steroid-induced cardiac contractility requires exogenous glucose,glycolysis and the sarcoplasmic reticulum in rainbow trout

Farrar

Battiprolu

Pierson

et al. 2006

Journal of Experimental Biology

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SUMMARY Recent data from our laboratory suggest that sex steroids promote contractile function in cardiac muscle of rainbow trout (Oncorhynchus mykiss Walbaum), and there are sex differences in hormone signaling and cardiac function. The current study investigated whether steroid-induced inotropism in electrically paced (0.5 Hz, 14°C) ventricle strips at 90%Lmax (1) has a metabolic requirement for exogenous glucose and (2) is associated with enhanced intracellular Ca2+ storage and release from the sarcoplasmic reticulum (SR). We also explored whether sex differences exist in extracellular Ca2+(Ca2+o) or cardiac sensitivity to Ca2+o. In the absence or at low concentrations (1 or 2 mmol l-1) of exogenous glucose, resting tension and relaxation time were increased selectively in cardiac tissue from females. Increasing glucose promoted twitch force in a bell-shaped manner, with 5 mmol l-1representing the optimal concentration for both sexes. The positive inotropic effects of physiological concentrations of testosterone (T) and 17β-estradiol (E2) in male and female trout ventricle strips,respectively, developed slowly (10-45 min) and were not apparent in glucose-free medium, in medium containing iodoacetate (IAA), an inhibitor of glycolysis, or medium containing 5 mmol l-1 lactate or pyruvate. Male ventricle strips had increased inotropic responses to glucose and T compared with female strips exposed to glucose and E2. Furthermore, sexually maturing males showed a greater inotropic response than immature males or females. Pretreatment with ryanodine (a specific blocker of SR Ca2+release) also eliminated the inotropic effects of sex steroids and exogenous glucose and reduced the post-rest potentiation of contractile force (a marker of SR Ca2+ storage). By contrast, the inotropic effects of epinephrine (Epi) or elevated Ca2+o were faster(developing within 1-3 min) and were not diminished by the presence or absence of glucose or by pretreatment with IAA or ryanodine. Sex differences were also found in responsiveness to caffeine (males > females) and the relationship between Ca2+ concentration and force development above baseline. The Ca2+50 was lower in female cardiac tissue than males, suggesting greater Ca2+ sensitivity, and although plasma albumin was higher in females, total and ionized plasma Ca2+ did not differ between the sexes. For the first time, our study highlights the importance of extracellular glucose, glycolytic activity and SR Ca2+ storage and release for sex steroid-induced inotropism in the trout ventricle. Conversely, the inotropes Epi and elevated[Ca2+o] do not require the presence or metabolism of exogenous glucose or the SR for signaling their positive effects on contractility. These results also demonstrate novel sex-related differences in cardiac reliance on exogenous glucose, Ca2+ sensitivity and SR function and thus should be considered in future studies.

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“…In Fig. 3.3.2, rate of increase in Fura-2/Rhod-2 fluorescence following caffeine application was little bit slower and did not resume the baseline probably due to the slow activity of the mitochondrial Na + /Ca 2+ exchanger, the major pathway for mitochondrial Ca 2+ efflux, as has previously been reported clearly in other articles (Leoty et al, 2001). Experimental observations during different pharmacological conditions support the concept that the presence of mSOD1 G93A severely disrupts itochondrial Ca 2+ regulation.…”

Section: Mechanism Underlying Mitochondria-er Ca 2+ Stores Couplingsupporting

confidence: 65%

Optical Analysis of [Ca2+]i and Mitochondrial Signaling Pathways: Implications for the Selective Vulnerability of Motoneurons in Amyotrophic Lateral Sclerosis (ALS)

Kumar¹

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Caffeine stimulates the reverse mode of Na⁺/Ca²⁺ exchanger in ferret ventricular muscle

Cited by 6 publications

References 22 publications

Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease

Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease

Steroid-induced cardiac contractility requires exogenous glucose,glycolysis and the sarcoplasmic reticulum in rainbow trout

Optical Analysis of [Ca<sup>2+</sup>]i and Mitochondrial Signaling Pathways: Implications for the Selective Vulnerability of Motoneurons in Amyotrophic Lateral Sclerosis (ALS)

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