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Intracellular Na+ Concentration (intracellular + na+_concentration)
Selected AbstractsReduced calcium tolerance in rat cardiomyocytes after myocardial infarctionACTA PHYSIOLOGICA, Issue 4 2002I. Sjaastad ABSTRACT During ischaemia and reperfusion the intracellular Na+ concentration is elevated in the cardiomyocytes and the cells are depolarized, both favouring reverse mode Na,Ca-exchange loading of the cell with Ca2+. We examined whether cardiomyocytes from rats with congestive heart failure (CHF) and younger rats (HINCX) which both have a high expression of the Na,Ca-exchanger protein (NCX) showed reduced tolerance to extracellular Ca2+. The CHF was induced in Isofluran anaesthetized rats by left coronary artery ligation. Isolated cardiomyocytes were loaded with Fura-2AM and 140 mm Na+ and exposed to 0.05 mm Ca2+. Expression of the Na,Ca-exchanger protein was analysed. Fura-2 340/380 ratio rose more rapidly in HINCX and CHF than in SHAM, and the rise was abolished by Ni2+. Hypercontracture developed more frequently in HINCX and CHF than in SHAM cells. The amount of NCX was 54% higher in HINCX and 76% higher in CHF compared with SHAM. Na+ -loaded cardiomyocytes from CHF and HINCX rats are more susceptible to Ca2+ overload than SHAM cells because of the increased capacity for Na,Ca-exchange. [source] 5-hydroxytryptamine-mediated increase in glutamate uptake by the leech giant glial cellGLIA, Issue 8 2006Ingolf C. Hirth Abstract The clearance of synaptically released glutamate is one of the pivotal functions of glial cells. We have studied the role of 5-hydroxytryptamine (5-HT, 30 ,M), a neurotransmitter and neurohormone in the leech central nervous system with a versatile action spectrum, on the efficacy of glial glutamate uptake. The activity of the glutamate uptake carrier in the giant glial cell in isolated ganglia of Hirudo medicinalis was monitored by measuring the membrane current and the change in the intracellular Na+ concentration (Na+i) as induced by the glutamate carrier substrate D -aspartate (D -asp, 1 mM). 5-HT increased the D -asp-induced current (EC50 at 5 ,M) and rise in Na+i, an effect which was mimicked by the membrane-permeable cyclic nucleotide analogue dibutyryl-cyclic AMP (db-cAMP). The adenylyl cyclase inhibitor SQ 22,536 and the protein kinase A antagonist Rp-cAMP inhibited the effect of 5-HT. Blocking the G protein in the giant glial cell by injecting GDP-,-S suppressed the effect of 5-HT, but not the effect of db-cAMP, on the D -asp-induced current. Our results suggest that 5-HT enhances the glial uptake of glutamate via cAMP- and PKA-mediated pathway. © 2006 Wiley-Liss, Inc. [source] Mechanism of the persistent sodium current activator veratridine-evoked Ca2+ elevation: implication for epilepsyJOURNAL OF NEUROCHEMISTRY, Issue 3 2009Ádám Fekete Abstract Although the role of Na+ in several aspects of Ca2+ regulation has already been shown, the exact mechanism of intracellular Ca2+ concentration ([Ca2+]i) increase resulting from an enhancement in the persistent, non-inactivating Na+ current (INa,P), a decisive factor in certain forms of epilepsy, has yet to be resolved. Persistent Na+ current, evoked by veratridine, induced bursts of action potentials and sustained membrane depolarization with monophasic intracellular Na+ concentration ([Na+]i) and biphasic [Ca2+]i increase in CA1 pyramidal cells in acute hippocampal slices. The Ca2+ response was tetrodotoxin- and extracellular Ca2+ -dependent and ionotropic glutamate receptor-independent. The first phase of [Ca2+]i rise was the net result of Ca2+ influx through voltage-gated Ca2+ channels and mitochondrial Ca2+ sequestration. The robust second phase in addition involved reverse operation of the Na+,Ca2+ exchanger and mitochondrial Ca2+ release. We excluded contribution of the endoplasmic reticulum. These results demonstrate a complex interaction between persistent, non-inactivating Na+ current and [Ca2+]i regulation in CA1 pyramidal cells. The described cellular mechanisms are most likely part of the pathomechanism of certain forms of epilepsy that are associated with INa,P. Describing the magnitude, temporal pattern and sources of Ca2+ increase induced by INa,P may provide novel targets for antiepileptic drug therapy. [source] High extracellular [Mg2+]-induced increase in intracellular [Mg2+] and decrease in intracellular [Na+] are associated with activation of p38 MAP kinase and ERK2 in guinea-pig heartEXPERIMENTAL PHYSIOLOGY, Issue 12 2008Shang-Jin Kim High extracellular Mg2+ concentrations ([Mg2+]o) caused a remarkable concentration-dependent and reversible increase in intracellular Mg2+ concentrations ([Mg2+]i) in beating and quiescent guinea-pig papillary muscles, accompanied by a definite decrease in intracellular Na+ concentrations ([Na+]i). A change in 1 mm[Mg2+]o evoked a direct change in 0.0161 mm[Mg2+]i and an inverse change in 0.0263 mm[Na+]i. Imipramine completely abolished the high [Mg2+]o -induced decrease in [Na+]i and remarkably diminished the high [Mg2+]o -induced increase in [Mg2+]i in papillary muscles. High [Mg2+]o also produced a significant activation of p38 mitogen-activated protein (MAP) kinase and extracellular signal-related kinase 2 (ERK2) that was inhibited by pretreatment with imipramine. These results suggest that the high [Mg2+]o -induced increase in [Mg2+]i could be coupled with the decrease in [Na+]i, which might involve activation of the reverse mode of Na+,Mg2+ exchange, accompanied by activation of p38 MAP kinase and ERK2 in the guinea-pig heart. [source] NANOMOLAR LEVEL OF OUABAIN INCREASES INTRACELLULAR CALCIUM TO PRODUCE NITRIC OXIDE IN RAT AORTIC ENDOTHELIAL CELLSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004Xian Hui Dong Summary 1.,Changes in [Ca2+]i across the cell membrane and/or the sarcoplasmic reticulum regulate endothelial nitric oxide (NO) synthase activity. 2.,In the present study, we investigated the effect of ouabain, a specific inhibitor of Na+/K+ -ATPase, on NO release and [Ca2+]i movements in cultured rat aortic endothelial cells (RAEC) by monitoring NO production continuously using an NO-specific real-time sensor and by measuring the change in [Ca2+]i using a fluorescence microscopic imaging technique with high-speed wavelength switching. The t˝ (half-time of the decline of [Ca2+]i to basal levels after stimulation with 10 µmol/L bradykinin) was used as an index of [Ca2+]i extrusion. 3.,A very low concentration of ouabain (10 nmol/L) did not increase the peak of NO production, but decreased the decay of NO release and, accordingly, increased integral NO production by the maximal dose,response concentration induced by bradykinin. The same dose of ouabain affected [Ca2+]i movements across the cell membrane and/or sarcoplasmic reticulum induced by bradykinin with a time-course similar to that of NO release. Moreover, the t˝ was significantly increased. 4.,Pretreatment of RAEC with Na+ -free solution, an inhibitor of the Na+/Ca2+ exchanger, and nickel chloride hexahydrate prevented the effects induced by bradykinin and ouabain. 5.,These observations using real-time recording indicate that a small amount of ouabain contributes to the bradykinin-stimulated increase of NO production through inhibition of plasma membrane Na+/K+ -ATPase activity and an increase in intracellular Na+ concentrations. The membrane was then depolarized, leading to a decline in the bradykinin-stimulated increase in [Ca2+]i by forward mode Na+/Ca2+ exchange to prolong the Ca2+ signal time. 6.,From these results, we suggest that nanomolar levels of ouabain modulate [Ca2+]i movements and NO production in RAEC. [source] | ||||||||||