ライフサイエンスコーパス: Ca2 uptake

1 s release of mitochondrial Ca2+ and prevents Ca2+ uptake.

2 ired for optimal activation of mitochondrial Ca2+ uptake.

3 O. produced by SR-associated NOS inhibits SR Ca2+ uptake.

4 s not directly involved in A beta P-mediated Ca2+ uptake.

5 cts are mediated by changes in mitochondrial Ca2+ uptake.

6 urther increasing cytosolic Ca2+ by reducing Ca2+ uptake.

7 ng depolarization, may involve mitochondrial Ca2+ uptake.

8 ng site is responsible for the inhibition of Ca2+ uptake.

9 not directly involved in the AbetaP-mediated Ca2+ uptake.

10 e-induced Ca2+ release, without affecting SR Ca2+ uptake.

11 exon, cAMP failed to regulate Na+-dependent Ca2+ uptake.

12 -ATPase activity paralleled their effects on Ca2+ uptake.

13 I may have stimulatory effects on ICa and SR Ca2+ uptake.

14 en prolonged Ca2+ transients, and augment SR Ca2+ uptake.

15 ly implicated in mating pheromone-stimulated Ca2+ uptake.

16 ecrease in [Ca2+] within the bath, due to SR Ca2+ uptake.

17 a2+ efflux pathway rather then inhibition of Ca2+ uptake.

18 tochondrial membrane potential and decreased Ca2+ uptake.

19 pling between Ca2+ release and mitochondrial Ca2+ uptake.

20 nel sensitive to inhibitors of mitochondrial Ca2+ uptake.

21 secondary to Ca2+-dependent activation of SR Ca2+ uptake.

22 and demonstrates a role for TRPC3 in apical Ca2+ uptake.

23 e uniporter responsible for energy-dependent Ca2+ uptake.

24 ndently published data sets on mitochondrial Ca2+ uptake.

25 ation within the SR, resulting in maintained Ca2+ uptake.

26 2+ without further increase in mitochondrial Ca2+ uptake.

27 induced a significant (P < 0.05) increase in Ca2+ uptake accompanied by membrane depolarization (9 mV

28 investigated how inhibition of mitochondrial Ca2+ uptake affects transmitter release from mouse motor

29 store [Ca2+] signals as greatly accelerated Ca2+ uptake after Ca2+ release from internal stores.

30 The kinetics of microsomal Ca2+ uptake after phospholamban phosphorylation or tryps

31 Mitochondrial Ca2+ uptake also increases the dynamic range over which

32 (iii) Impaired mitochondrial Ca2+ uptake alters the spatiotemporal characteristics of

33 Impaired sarcoplasmic reticular (SR) Ca2+ uptake and a greater dependence on Na+/Ca2+ exchang

34 have a higher capacity for energy-dependent Ca2+ uptake and a greater resistance to Ca(2+)-induced r

35 Ts) temperature-sensitive growth which block Ca2+ uptake and accumulation, suggesting that cytosolic

36 acellular Na+ ([Na+]i) affects mitochondrial Ca2+ uptake and bioenergetics.

37 + overload by reducing the driving force for Ca2+ uptake and by activating cyclosporin-sensitive Ca2+

38 cid (EC50 approximately 3 microM) stimulated Ca2+ uptake and calcium-activated ATP hydrolysis at subm

39 Quercetin had a biphasic effect on Ca2+ uptake and calcium-stimulated ATP hydrolysis in iso

40 opsis thaliana rhd2 mutants are defective in Ca2+ uptake and consequently cell expansion is compromis

41 rotein exhibit a defect in pheromone-induced Ca2+ uptake and consequently lose viability upon mating

42 mic reticulum, because endoplasmic reticulum Ca2+ uptake and content were reduced in betaIRS1-A cells

43 ances, however, are active in modifying both Ca2+ uptake and efflux through oat and pea leaf protopla

44 lism, and the possibility that mitochondrial Ca2+ uptake and extrusion modulate free cytosolic [Ca2+]

45 Measuring both 12-min Ca2+ uptake and initial Ca2+ uptake rates, the apparent

46 In contrast, Ca2+ uptake and InsP3-independent Ca2+ release were very

47 ons, suggesting that the activity of both SR Ca2+ uptake and Na(+)-Ca2+ exchange is affected by lacta

48 Under these conditions, mitochondrial Ca2+ uptake and Na+/Ca2+ exchange do not significantly i

49 effect of NO depended on the initial rate of Ca2+ uptake and on the concentration of ATP and was abol

50 oss the inner mitochondrial membrane blocked Ca2+ uptake and pacemaker currents in cultured ICC and b

51 a2+ load mechanistically due to increased SR Ca2+ uptake and reduced SR Ca2+ leak.

52 , these knockdown myotubes exhibited reduced Ca2+ uptake and reduced stored Ca2+ release by UTP (400

53 nctions, several inhibitors of mitochondrial Ca2+ uptake and release (tetraphenylphosphonium or TPP+,

54 Thapsigargin (5 microM) prevented Ca2+ uptake and release by the sarcoplasmic reticulum.

55 ) the plasma membrane electrophysiology; (b) Ca2+ uptake and release from the sarcoplasmic reticulum

56 was prevented by inhibitors of mitochondrial Ca2+ uptake and release mechanisms.

57 tary time courses of mitochondrial versus ER Ca2+ uptake and release suggest that these organelles pa

58 Inhibitors of Ca2+ influx, SR Ca2+ uptake and release, mitochondrial Ca2+ uptake, mito

59 In contrast, 20 mM oxalate increased Ca2+ uptake and the [Ca2+] within the bath continued to

60 not due to a change in the driving force for Ca2+ uptake and therefore must be due to an enhanced Ca2

61 d Ca2+ release without affecting the rate of Ca2+ uptake and/or extrusion.

62 nsiently cease without affecting the rate of Ca2+ uptake and/or extrusion.

63 hat evoke[Ca2+]i oscillations, mitochondrial Ca2+ uptake, and a nuclear [Ca2+] delay, CCh also evoked

64 ed cardiac myocyte SERCA2 levels, augment SR Ca2+ uptake, and shorten prolonged excitation-contractio

65 he Ca2+ current; (ii) sarcoplasmic reticulum Ca2+ uptake; and (iii) mRNA expression of important comp

66 .1 mM), completely inhibited the PCP-induced Ca2+ uptake as well as the membrane depolarization eithe

67 Ca2+ uptake assays in a membrane preparation indicated a

68 Ca2+ uptake assays showed 44+/-8% reduction of Vmax in c

69 Sarcoplasmic reticulum Ca2+ uptake assays showed that the Vmax was decreased by

70 Maintained Ca2+ uptake associated with Ca-Pi precipitation was not

71 establishment of MCU-dependent mitochondrial Ca2+ uptake at glutamatergic synapses rescues the altere

72 L6, but not Jurkat cells, inhibited Ca2+ uptake at very high Ca2+ concentrations.

73 Mn2+ until the point at which mitochondrial Ca2+ uptake became apparent.

74 FK-506 did not affect SR Ca2+ uptake but modestly decreased Ca2+ extrusion via Na

75 line of [Ca2+]SR was not due to decreased SR Ca2+ uptake, but instead was the result of increased SRC

76 Pi inhibits net SR Ca2+ uptake, but this appears to result from activation

77 Ca2+ release occurred after abolition of SR Ca2+ uptake by ATP withdrawal.

78 ugmented store-operated channel activity and Ca2+ uptake by intracellular organelles.

79 Inhibition of Ca2+ uptake by mitochondria did not change the effects o

80 was inhibited by ruthenium red, a blocker of Ca2+ uptake by mitochondria.

81 exin V liposomes, are blocked by Zn2+, as is Ca2+ uptake by MV incubated in synthetic cartilage lymph

82 the mechanism of inhibition of mitochondrial Ca2+ uptake by Ru360 and its specificity in vitro in iso

83 Despite their polarized expression, Ca2+ uptake by SERCA pumps and Ca2+ efflux by PMCA resul

84 ld be dysregulated at the level of cytosolic Ca2+ uptake by SERCA2a, its inhibitory subunit (phosphol

85 Inhibition of SR Ca2+ uptake by thapsigargin in cells already preloaded w

86 ased cytosolic Ca2+ was due to inhibition of Ca2+ uptake by the endoplasmic reticulum, because endopl

87 associated with mislocalization and reduced Ca2+ uptake by the mitochondria of stimulated Mist1-/- c

88 These data demonstrate that Ca2+ uptake by the mitochondria suppresses the local pos

89 Ca2+ uptake by the mitochondrial store is sensitive (thr

90 In contrast, inhibition of Ca2+ uptake by the sarcoplasmic reticulum ATPase does no

91 This does not depend on Ca2+ uptake by the sarcoplasmic reticulum but may reflec

92 Inhibition of Ca2+ uptake by the sarcoplasmic reticulum with cyclopiaz

93 d Ca2+ transient is dependent on the rate of Ca2+ uptake by the SR and (ii) prolongation associated w

94 A reduction in the rate of net Ca2+ uptake by the SR slows the decay of the Ca2+ transi

95 l membranes and that excessive mitochondrial Ca2+ uptake can impair electron transport and oxidative

96 rebellar granule cells demonstrated a higher Ca2+ uptake capacity (686 +/- 71 nmol/mg protein) than t

97 expressing cells had a reduced mitochondrial Ca2+ uptake capacity in comparison with wild type cells.

98 mPTP opening, were necessary to increase the Ca2+ uptake capacity of synaptic versus nonsynaptic mito

99 -induced Ca2+ load was less than the maximal Ca2+ uptake capacity of the mitochondria determined in v

100 pression of bcl-2 enhanced the mitochondrial Ca2+ uptake capacity using either digitonin-permeabilize

101 in the presence of ADP and the decreases in Ca2+ uptake capacity were abolished in the presence of P

102 Ca2+ was a smaller percentage of the maximal Ca2+ uptake capacity.

103 Mitochondrial Ca2+ uptake controls the rate of energy production, shap

104 LCT1-dependent increase in Ca2+ uptake correlated with the observed phenotype.

105 phore uncoupler that decreases mitochondrial Ca2+ uptake, decreased K+on but not K+off.

106 was most probably mediated by an enhanced SR Ca2+ uptake due to an augmentation of mitochondria-depen

107 f divalent cations, also are likely sites of Ca2+ uptake during contraction and the first step in con

108 Mitochondrial Ca2+ uptake during depolarizing stimulation caused depol

109 ermore, NOS blockade increased mitochondrial Ca2+ uptake during NMDA.

110 erated map analysis revealed that because SR Ca2+ uptake efficiency was much higher in control atrial

111 Pore opening does not occur following Ca2+ uptake, even though ruthenium red-inhibited rat liv

112 e the consequences of impaired mitochondrial Ca2+ uptake for cell function?' and finally (iv) 'What a

113 mately 10.8-fold, indicating active, dynamic Ca2+ uptake from cytosol into the granules.

114 increased pump levels result in increased SR Ca2+ uptake function.

115 beta-Adrenergic stimulation of SR Ca2+ uptake in cells from failing hearts sufficed only t

116 Mitochondrial Ca2+ uptake in combination with NO production triggers t

117 hatase) corrected [Ca2+]er and mitochondrial Ca2+ uptake in DKO cells, restoring apoptotic death in r

118 acemaker currents and rhythmic mitochondrial Ca2+ uptake in ICC were also blocked by inhibitors of IP

119 s studied on the membrane potential (Vm) and Ca2+ uptake in isolated single skeletal muscle cells of

120 These data suggest that mitochondrial Ca2+ uptake in response to an increase of cytosolic Ca2+

121 ore expression caused enhanced mitochondrial Ca2+ uptake in response to ER Ca2+ release induced by th

122 nts of a yeast Ca2+ channel that may mediate Ca2+ uptake in response to mating pheromone, salt stress

123 l distribution and the role of mitochondrial Ca2+ uptake in shaping the spatial and temporal properti

124 t on the 10-min time course of ATP-dependent Ca2+ uptake in the absence of the luminal Ca2+ chelator

125 t cations such as Li+, suggesting a role for Ca2+ uptake in the calcineurin-dependent ion stress resp

126 Bcl-2 overexpression maintains Ca2+ uptake in the ER of TG-treated cells and prevents a

127 It also inhibits ATP-dependent Ca2+-uptake in a variety of microsomal membranes, althou

128 by manipulations that blocked mitochondrial Ca2+ uptake, including replacement of extracellular Ca2+

129 mycin on Ca2+ release evoked by agonists and Ca2+ uptake induced by antagonists.

130 Mitochondrial Ca2+ uptake inhibition prevented the NO increase, wherea

131 educed in cells treated with a mitochondrial Ca2+ uptake inhibitor, carbonyl cyanide m-chlorophenylhy

132 s (pool 1) and perpetuated through cycles of Ca2+ uptake into and release from Ca2+-induced Ca2+ rele

133 ctifying, making it especially effective for Ca2+ uptake into energized mitochondria.

134 ellular Ca2+ pools by blocking LTP-dependent Ca2+ uptake into intracellular compartments, blocked the

135 racellular acidosis is due to enhancement of Ca2+ uptake into intracellular stores as a result of a r

136 asmic reticulum Ca2+-ATPase (SERCA)-mediated Ca2+ uptake into intracellular stores is also accelerate

137 zonic acid (CPA, 20-40 microM), a blocker of Ca2+ uptake into intracellular stores.

138 ns of Ca(2+)-releasing agonists by promoting Ca2+ uptake into intracellular stores.

139 We conclude that Ru360 specifically blocks Ca2+ uptake into mitochondria and can be used in intact

140 responses were recorded from cells in which Ca2+ uptake into mitochondria had been inhibited by micr

141 ltage-clamped ventricular myocytes prevented Ca2+ uptake into mitochondria in situ where the cells we

142 However, the specificity of Ru360 on Ca2+ uptake into mitochondria in vitro or in intact cell

143 Ruthenium red is a well known inhibitor of Ca2+ uptake into mitochondria in vitro.

144 However, its utility as an inhibitor of Ca2+ uptake into mitochondria in vivo or in situ in inta

145 The IC50 of 103Ru360 for the inhibition of Ca2+ uptake into mitochondria was also 0.2 nM, indicatin

146 ruthenium red (IC50 = 6.85 nM) in inhibiting Ca2+ uptake into mitochondria.

147 chloride channels appears to be regulated by Ca2+ uptake into mitochondria.

148 s in ciliated cells are caused by stimulated Ca2+ uptake into mitochondria.

149 Ca2+ uptake into some mitochondria is activated by Ca2+

150 pH did not affect the rate of ATP-dependent Ca2+ uptake into stores, but did modify the rate of Ca2+

151 doplasmic reticulum) of isolated microsomes, Ca2+ uptake into streptolysin O-permeabilized cells, and

152 ns in a manner consistent with inhibition of Ca2+ uptake into the endoplasmic reticulum.

153 ment with thapsigargin (TG), an inhibitor of Ca2+ uptake into the endoplasmic reticulum.

154 inacidil decreased the rate and magnitude of Ca2+ uptake into the mitochondrial matrix with an IC50 o

155 influx via L-type Ca2+ current and stimulate Ca2+ uptake into the sarcoplasmic reticulum (SR), thereb

156 that SERCA2 protein and maximal velocity of Ca2+ uptake into the sarcoplasmic reticulum were reduced

157 2+ influx in intact platelets and to monitor Ca2+ uptake into the stores in permeabilized platelets,

158 + content of internal stores, measurement of Ca2+ uptake into the thapsigargin- and oxalate-sensitive

159 This suggests that SR Ca2+ uptake is balanced by an efflux under these conditi

160 Mitochondrial Ca2+ uptake is critical for wave propagation, and mitoch

161 Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release,

162 ate that maximal activation of mitochondrial Ca2+ uptake is evoked by IP3-induced perimitochondrial [

163 This suggests that SR Ca2+ uptake is faster in these myocytes.

164 Thus, SR Ca2+ uptake is markedly downregulated in failing hearts,

165 ar and platelet microsomes, a stimulation in Ca2+ uptake is observed at low curcumin concentrations (

166 The rate of mitochondrial Ca2+ uptake is sensitive to extracellular [Ca2+], indica

167 ggesting that the net sarcoplasmic reticulum Ca2+ uptake is smaller in the presence of lactate.

168 This Ca2+ uptake is undertaken by the mitochondrial Ca2+ unip

169 ss induced by t-BuOOH enhances mitochondrial Ca2+ uptake, leading to increased matrix Ca2+, increased

170 We find that mitochondrial Ca2+ uptake limits the rise and underlies the rapid deca

171 This proficient mitochondrial Ca2+ uptake may avert a large rise in cytosolic Ca2+ con

172 ns high for long enough, while mitochondrial Ca2+ uptake may be important when [Ca2+]i is high.

173 t perinuclear mitochondria and mitochondrial Ca2+ uptake may differentially shape nuclear [Ca2+] sign

174 ciation with oxidative stress, mitochondrial Ca2+ uptake may trigger pathological states that lead to

175 mitochondrial Ca2+ uniporter is the primary Ca2+ uptake mechanism in respiring mitochondria.

176 sympathetic ganglion neurons exhibit a novel Ca2+ uptake mechanism, release-activated calcium transpo

177 d the maximal rate of thapsigargin-sensitive Ca2+ uptake mediated by SERCA in sarcoplasmic vesicles a

178 x, SR Ca2+ uptake and release, mitochondrial Ca2+ uptake, mitochondrial permeation transition pore, c

179 SR in the pathogenesis of HF, with abnormal Ca2+ uptake, more than Ca2+ release, contributing to the

180 ?' (ii) 'What is the impact of mitochondrial Ca2+ uptake on Ca2+ signalling?' (iii) 'What are the con

181 ns: (i) 'What is the impact of mitochondrial Ca2+ uptake on mitochondrial function?' (ii) 'What is th

182 epresent a first plant cDNA encoding a plant Ca2+ uptake or an organellar Ca2+ transport pathway in p

183 mpared with other interventions that inhibit Ca2+ uptake or reduce the sensitivity of the SR Ca2+ rel

184 produced no effect on sarcoplasmic reticulum Ca2+ uptake or release, sarcolemmal Na+/Ca2+ exchange, a

185 lum Ca2+-ATPase, disruption of mitochondrial Ca2+ uptake, or inhibition of the Na+-Ca2+ exchanger did

186 A number of specific cellular Ca2+ uptake pathways have been described in many differe

187 ial membrane potential (DeltaPsim)-dependent Ca2+ uptake plays a central role in neurodegeneration af

188 In conclusion, mitochondrial Ca2+ uptake plays a major role in Ca2+ clearance by rapi

189 Consequently, mitochondrial Ca2+ uptake plays a substantial role in shaping [Ca2+]c

190 ge-clamp technique to ascertain whether this Ca2+ uptake process influences the time course of the su

191 in, and triadin) were downregulated, whereas Ca2+-uptake proteins (Ca2+-ATPase and phospholamban) wer

192 pensate for depressed sarcoplasmic reticular Ca2+ uptake, provide inotropic support through reverse-m

193 iazonic acid (CPA), a sarcoplasmic reticulum Ca2+ uptake pump inhibitor.

194 iazonic acid (CPA), a sarcoplasmic reticulum Ca2+-uptake pump inhibitor.

195 mM oxalate resolved a thapsigargin-sensitive Ca2+ uptake rate (IC50 approximately 1 nM thapsigargin)

196 At very low [ATP], a reduction in the SR Ca2+ uptake rate may also contribute to the decrease in

197 d the Ca2+ transient, SR Ca2+ content and SR Ca2+ uptake rate to the same levels as control cells in

198 rawal may also reflect a decrease in the net Ca2+ uptake rate.

199 Ca2+ uptake rates by the SR and the amount of Ca2+ store

200 easuring both 12-min Ca2+ uptake and initial Ca2+ uptake rates, the apparent thapsigargin sensitivity

201 CA pump for Ca2+ and the maximum velocity of Ca2+ uptake rates.

202 d by mitochondrial depolarization, swelling, Ca2+ uptake, reactive oxygen species production, and res

203 ee hypotheses were tested: (1) Mitochondrial Ca2+ uptake regulates [Ca2+]i and production of force in

204 , cytosolic Ca2+ increase, and mitochondrial Ca2+ uptake remain obscure.

205 Mitochondrial Ca2+ uptake responds dynamically and sensitively to chan

206 fluctuations were triggered by mitochondrial Ca2+ uptake since they were inhibited by both ruthenium

207 We conclude that each mitochondrial Ca2+ uptake site faces multiple IP3R, a concurrent activ

208 anced Ca2+ permeability of the mitochondrial Ca2+ uptake sites (uniporter).

209 of high [Ca2+], saturation of mitochondrial Ca2+ uptake sites by released Ca2+, connection of multip

210 may utilize activation of the mitochondrial Ca2+ uptake sites by the large local [Ca2+]c rise occurr

211 n SR/ER Ca2+ release sites and mitochondrial Ca2+ uptake sites, including transient microdomains of h

212 However, after mitochondrial Ca2+ uptake starts, mitochondria continually take up Mn2

213 e roles of the L-type Ca2+ current (ICa), SR Ca2+ uptake, storage and release, Ca2+ transport via the

214 inal free [Ca2+] after inhibition of further Ca2+ uptake, submaximal concentrations of InsP3 caused r

215 fter inhibition of the endoplasmic reticulum Ca2+ uptake system (SERCA).

216 ger and inhibition of a pheromone-stimulated Ca2+ uptake system, suggesting that Tcn1p functions down

217 types, as expected after removal of a major Ca2+ uptake system.

218 ity in pancreatic islets, which mediates the Ca2+ uptake that triggers insulin secretion.

219 re the procedures to specifically measure SR Ca2+ uptake, the formation and decomposition of SERCA ph

220 released Ca2+ is modulated by mitochondrial Ca2+ uptake, the interactions between ER and mitochondri

221 At all stages of Ca2+ uptake, the potassium channel openers depolarized t

222 d the mitochondrial energization that drives Ca2+ uptake through it.

223 ll and coupling Ca2+ entry and mitochondrial Ca2+ uptake to Ca2+ release.

224 m promoting quiescence via BK channels or SR Ca2+ uptake, to promoting Ca2+ entry and contractility a

225 ANT plays an important role in mitochondrial Ca2+ uptake under ischemic conditions by reversing its a

226 potential and unidirectional measurements of Ca2+ uptake using 45Ca2+.

227 e that core directly increases mitochondrial Ca2+ uptake via a primary effect on the uniporter.

228 The maximum velocity of Ca2+ uptake (Vmax) was increased by 37%, demonstrating t

229 The threshold [Ca2+]c for mitochondrial Ca2+ uptake was 300-500 nM, similar to that without Mn2+

230 Mitochondrial Ca2+ uptake was also dependent on the nature and duratio

231 34.5% augmentation of oxalate-facilitated SR Ca2+ uptake was also documented in SERCA2 adenovirus-inf

232 F, respectively, revealed that mitochondrial Ca2+ uptake was also inhibited by ruthenium red and Ru36

233 d [Ca2+]m by 0.2 microM, total mitochondrial Ca2+ uptake was approximately 13 mumol (1 mitochondria)-

234 bmaximal IP3 was enhanced when mitochondrial Ca2+ uptake was blocked with ruthenium red or uncoupler.

235 Mitochondrial Ca2+ uptake was calculated from the difference between [

236 Mitochondrial Ca2+ uptake was dependent on glutamate concentration, wh

237 reased 2.5-fold, and the maximal velocity of Ca2+ uptake was increased 1.7-fold in TG hearts, demonst

238 tage-clamped cells show that the PCP-induced Ca2+ uptake was independent of the PCP-induced depolariz

239 ation that MT-AEQ was in a compartment whose Ca2+ uptake was inhibited 82% with carbonyl cyanide p-tr

240 When mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria w

241 Net Ca2+ uptake was markedly reduced in the presence of 30 m

242 red treatment, suggesting that mitochondrial Ca2+ uptake was required for the mechanism of action.

243 The initial rate of Ca2+ uptake was similar in microsomes from transfected a

244 +/- 1.4% (mean +/- s.e.m., n = 16), while SR Ca2+ uptake was unaffected.

245 razone (CCCP), an inhibitor of mitochondrial Ca2+ uptake, was investigated on the properties of Ca(2+

246 DeltaPsim dissipation reduces mitochondrial Ca2+ uptake, we hypothesized that NO mediates the NMDA-i

247 store-operated Ca2+ entry, and mitochondrial Ca2+ uptake, we used two IP3-binding proteins (IP3BP): 1

248 sphosphate (IP3) receptors and mitochondrial Ca2+ uptake were tested on the generation of slow waves

249 Inhibition of mitochondrial Ca2+ uptake with cyanide, carbonyl cyanide p-trifluorome

250 Inhibition of SR Ca2+ uptake with cyclopiazonic acid (CPA, 30 microM) slo

251 Inhibition of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effe

252 was abolished by inhibition of mitochondrial Ca2+ uptake with ruthenium red and Ru360.

253 Inhibition of sarcoplasmic reticulum Ca2+ uptake with thapsigargin (100 nM) reduced the under

254 nd (2) elevated [Na+]i impairs mitochondrial Ca2+ uptake, with consequent effects on energy supply an