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At least 397 records · Page 22Linked to original sources
PubMed1988

Modulation by cytosolic pH of calcium and rubidium fluxes in rat pancreatic islets.

Cytosolic pH (pHi) of pancreatic islet cells was assessed using the fluorescent dye 2'7'-biscarboxyethyl-5'(6')-carboxyfluorescein (BCECF). pHi was rapidly lowered by addition of the sodium salt of a weak acid or by treatment with amiloride. In the latter case, no recovery of pHi occurred. NH4Cl produced a rise in pHi. Stimulation of islet cells with glyceraldehyde produced a sustained fall in pHi, whereas glucose and alpha-ketoisocaproate caused a small, gradual rise in pHi. Intracellular acidification, particularly with amiloride, resulted in an immediate potentiation of glucose-induced insulin secretion from perifused islets. In the case of weak acid treatment, subsequent removal of the weak acid produced a paradoxical stimulation of insulin release which was not observed upon removal of amiloride. NH4Cl produced a transient stimulation followed by a reduction in the rate of glucose-induced insulin secretion. A reduction in pHi, either in response to weak acid or amiloride treatment, was associated with a diminution in the rate of efflux of 86Rb+ and of 45Ca2+. Removal of weak acid produced a marked "rebound" stimulation of 86Rb+ and 45Ca2+ efflux. Treatment of islets with NH4Cl, either in the presence or absence of glucose or Ca2+, resulted in a marked stimulation of efflux of 86Rb+ and 45Ca2+. The stimulatory effect of NH4Cl on 45Ca2+ efflux was markedly impaired in the absence of Na+. It is concluded that pHi can influence the secretory activity of pancreatic islets, possibly via effects on potassium permeability and sodium-calcium exchange across the plasma membrane, resulting in altered mobilisation of calcium in the islet cell. However, it is unlikely that glucose or other nutrient stimuli activate islets solely via an effect on pHi.

Amiloride↗
PubMed1992

Interactions of trimethyl tin (TMT) with rat primary astrocyte cultures: altered uptake and efflux of rubidium, L-glutamate and D-aspartate.

Studies were undertaken to assess the effects of trimethyl tin (TMT) on metabolic functions in primary neonatal rat cultured astrocytes. Concentrations as low as 10(-5) M TMT significantly inhibited the initial rate (1 min) of uptake of 86RbCl, used as a tracer for K+. TMT also markedly inhibited the initial rate (1 min) of Na(+)-dependent uptake of L-[3H]glutamate and D-[3H]aspartate, and stimulated the release of intracellular 86Rb+, -[3H]glutamate and D-[3H]aspartate in a dose-dependent fashion. These observations support the hypothesis that the astrocyte plasma membrane is potentially an important target for TMT's toxic effect and specifically that small concentrations of this organometal can inhibit the ability of astrocytes to maintain a transmembrane K+ gradient. This would be expected to compromise the ability of astrocytes to control extracellular K+ either by spatial buffering or active uptake, and exacerbate on-going swelling. Increased levels of glutamate and aspartate in the extracellular fluid upon release from astrocytes may play an important role in TMT neurotoxicity.

Animals↗
PubMed1992

Effects of serotonin and carbachol on glial and neuronal rubidium uptake in leech CNS.

Effects of serotonin (5-HT) and carbachol on Rb uptake (used as a K marker) in leech neuron and glia were studied by electron probe microanalysis (EPMA). Hirudo medicinalis ganglia were perfused 60 s in 4 mM Rb substituted normal leech Ringer's with and without 5-HT (dosage range 5-500 microM) or carbachol (range 10-1000 microM), quench frozen cryosectioned, and subjected to EPMA to determine elemental mass fractions and cell water content. Both 5-HT and carbachol altered leech neuron and glial cell elemental distribution and water content. In glial cells, a dose-dependent increase in Rb uptake was observed following 5-HT (control: 26 +/- 2 microM; 5 microM: 47 +/- 4; 50 microM: 62 +/- 4; 500 microM: 82 +/- 11 mmol/kg dry wt. +/- S.E.M.) and carbachol (10 microM: 35 +/- 3; 100 microM: 52 +/- 3; 1000 microM: 68 +/- 3 mmol/kg dry wt. +/- S.E.M.). In neurons, 5-HT and carbachol had small effects. 5-HT decreased glial and neuronal cell water content. Carbachol decreased neuronal (but not glial) water content by approximately the same amount (mean decrease 9%) regardless of dose. Both 5-HT and carbachol affected glial cell K-accumulating properties, providing evidence that certain neurotransmitters may modulate invertebrate glial cells' K clearance function.

Animals↗
PubMed1992

Rubidium transport in cultured monkey retinal pigment epithelium.

Rb+ influx was used to assess Na-K-Cl cotransport and Na,K-ATPase activities in cultured monkey retinal pigment epithelium. Bumetanide-sensitive (Na-K-Cl cotransport-mediated) Rb+ influx exceeds ouabain-sensitive (Na,K-ATPase-mediated) Rb+ influx, with these two transporters accounting for approximately 95% of total Rb+ uptake. Half-maximal inhibition of Rb+ influx by bumetanide is attained at 75 nM bumetanide. The bumetanide-sensitive Rb+ influx depends on both extracellular Na+ and Cl-, and is activated by extracellular Rb+ with a relatively high affinity. Na-K-Cl cotransport activity is stimulated (2.5-fold) by increased extracellular osmolarity. Elevated cAMP content and glycolytic inhibition both depress cotransport activity. Cyanide application, however, had very little effect on Na-K-Cl cotransport activity. Monkey retinal pigment epithelial cells, maintained in culture, provide a system in which the activity and regulation of cation transport mechanisms can be examined.

Animals↗
PubMed1984

[3H]Ouabain binding and 86 rubidium uptake during the dimethyl sulfoxide-induced differentiation of human promyelocytic leukemia HL-60 cells.

When HL-60 cells were induced to differentiate into granulocyte-like cells by culture in the presence of 1.3% dimethyl sulfoxide, an increase in the rate of ouabain-sensitive 86Rb transport was observed during the first 6 h followed by a constant decrease which became stable on day 4 at about 40% of control level. By contrast, the number of ouabain binding sites remained constant during the first 24 h then decreased with the same kinetics as that of the 86Rb transport rate. These results suggest that alterations in ionic fluxes, through activation of the sodium pump, are part of the early events resulting in HL-60 cell differentiation.

Binding Sites↗