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PubMed1979

Vascular perfusion of the cochlea: effect of potassium-free and rubidium-substituted media.

By means of vascular perfusion of the cochlea with K+-free synthetic blood, it is possible to maintain the endocochlear potential (EP) at normal or supernormal levels for periods of 20-42 min. The subsequent decline of the EP is comparatively slow. This is in contrast to the immediate onset and rapid decline of the EP during perilymphatic perfusion with K+-free media. Possible implications of these data concerning the mode of generation of the EP are briefly discussed. It is further shown, that synthetic blood, in which K+ is replaced by Rb+, maintains the EP at normal or near normal levels for 2 h.

Cochlea↗
PubMed1984

Patch-clamp study of rubidium and potassium conductances in single cation channels from mammalian exocrine acini.

Single-channel current recordings were carried out on excised inside-out patches of baso-lateral plasma membrane from exocrine acinar cells. The mouse pancreas and submandibular gland as well as the pig pancreas were investigated. In the mouse pancreas the voltage-insensitive Ca2+-activated cation channel was studied. Single-channel current-voltage (i/v) relationships were studied in symmetrical Rb+-rich solutions and in asymmetrical Rb+/Na+ and Na+/Rb+ solutions. In all cases the i/v relations were linear and had the same slope representing a single-channel conductance of about 33 pS which is identical to that previously obtained with symmetrical Na+ solutions or asymmetrical Na+/K+ solutions. In the mouse submandibular gland and the pig pancreas the voltage and Ca2+-activated K+ channel was studied. The outward currents observed after depolarization in the presence of quasi-physiological Na+/K+ gradients were immediately abolished when all the K+ in the bath fluid was replaced by Rb+ (bath fluid in contact with inside of plasma membrane). This effect was immediately and fully reversible upon return to the high K+ solution. The voltage and Ca2+-activated K+ channel was also studied in asymmetrical K+/Rb+ and Rb+/K+ solutions. In the first case inward (K+) currents could be observed but not outward (Rb+) currents, while in the other case inward (Rb+) currents could not be seen whereas outward (K+) currents were measured. The current-voltage relationships were approximately linear and the null potential was close to 0 mV in both situations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of forskolin and analogues on nicotinic receptor-mediated sodium flux, voltage-dependent calcium flux, and voltage-dependent rubidium efflux in pheochromocytoma PC12 cells.

1. Forskolin, a naturally occurring diterpene that activates adenylate cyclase, HL706, a water-soluble derivative of forskolin (6 beta-[(piperidino)acetoxy]-7-desacetylforskolin) that is less potent than forskolin in activating adenylate cyclase, and 1,9-dideoxyforskolin, an analogue that does not activate adenylate cyclase, were examined for effects on the nicotinic receptor-mediated 22Na+ flux, a high potassium-induced 45Ca2+ flux through L-type calcium channels, and a high potassium-induced 86Rb+ efflux through a calcium-dependent potassium channels in PC12 cells. 2. Forskolin and analogues at 30 microM completely blocked carbamylcholine-elicited flux of 22Na+ through the nicotinic receptor-gated channel. 1,9-Dideoxyforskolin had an IC50 value of 1.6 microM with forskolin and HL706 being two- to three fold less potent. 3. Forskolin and its analogues appear to be noncompetitive blockers of the neuronal nicotinic receptor-channel complex in PC12 cells, but unlike many noncompetitive blockers, did not markedly enhance desensitization. Instead, forskolin, but not HL706 or 1,9-dideoxyforskolin, slightly antagonized the desensitization evoked by high concentrations of carbamylcholine. N-Ethylcarboxamidoadenosine, an adenosine analogue that elevates cyclic AMP and 8-bromo-cyclic AMP had no effect on desensitization. 4. Forskolin, HL706, and 1,9-dideoxyforskolin in the presence of carbamylcholine inhibited the binding of a noncompetitive blocker, [3H]perhydrohistrionicotoxin, to the muscle-type nicotinic receptor-channel complex in Torpedo electroplax membranes with IC50 values of 20 microM. Forskolin had no effect on [3H]perhydrohistrionicotoxin binding in the absence of carbamylcholine, while HL706 and 1,9-dideoxyforskolin still inhibited binding in the absence of carbamylcholine. 5. Forskolin, but not HL706 or 1,9-dideoxyforskolin had a slight inhibitory effect on the binding of [125I]alpha-bungarotoxin to acetylcholine recognition sites in Torpedo membranes. 1,9-Dideoxyforskolin at 30 microM, but not forskolin or HL706, markedly inhibited depolarization-evoked 45Ca+ flux and 86Rb+ efflux in PC12 cells, suggesting that 1,9-dideoxyforskolin has nonspecific inhibitory effects on a variety of ion channels.

Adrenal Gland Neoplasms↗
PubMed1993

Rubidium transport in irradiated vitamin-E-deficient bone marrow cells.

We showed previously that the Rb+ transport rate in bone marrow cells (BMC) of vitamin-E-deficient mice is significantly lower than that in BMC of euvitaminotic mice. It is now evident that 4 h after whole-body, low-dose (0.01-1.0 Gy) gamma-irradiation of avitaminotic mice, there is an increase in the rate of Rb+ transport. This increase is quite pronounced, exceeding at all dose levels the rate of Rb+ transport in euvitaminotic mice exposed to the same radiation dose.

Animals↗
PubMed1979

Alloxan-induced alteration of insulin release, rubidium efflux and glucose metabolism in rat islets stimulated by various secretagogues.

Insulin release and 86Rb efflux were studied in perifused rat islets exposed in vitro to alloxan (2 mmol/l) for 5 min. At a low glucose concentration, alloxan transiently increased 86Rb efflux. Alloxan immediately and completely abolished the secretory response to glucose (15 mmol/l) and markedly delayed the reduction in 86Rb efflux normally produced by the sugar. 3-O-methylglucose (20 mmol/l) provided complete protection against the alteration of 86Rb efflux and partial protection against the inhibition of insulin release. Immediately after alloxan treatment, glyceraldehyde, alpha-ketoisocaproic acid and tolbutamide still induced a rapid release of insulin, but the late phase normally stimulated by glyceraldehyde and alpha-ketoisocaproic acid was inhibited. If islets were exposed to glyceraldehyde or tolbutamide 15 min after alloxan treatment, the rapid insulin release was also markedly impaired. Alloxan failed, however, to affect the ability of these three stimuli to reduce 86Rb efflux from islet cells. Glucose oxidation and utilization were decreased in alloxan-treated islets and 3-O-methylglucose protected against this effect. The results show that the glucose recognition system in B-cells is the most rapidly and severely affected by alloxan. The drug also alters the response to other secretagogues, the insulin releasing properties of which can be impaired without alteration of their ability to reduce 86Rb efflux.

Alloxan↗
PubMed1982

The dual effect of rubidium ions on potassium efflux in depolarized frog skeletal muscle.

The effects of external Rb+ on the efflux of 42K+ from whole frog sartorius muscles loaded with 305 mM K+ and 120 mM Cl- were studied. K+ efflux is activated by [Rb+]o less than about 40 mM according to a sigmoid relation similar to that for activation by [K+]o. At [Rb+]o greater than 40 mM, K+ efflux declines, although at [Rb+]o = 300 mM it is still greater than at [Rb+]o = 0 mM. For low concentrations, the increment in K+ efflux over that in K+-and Rb+-free solution, delta K, is described by the relation delta k = a[X+]on, for both K+ and Rb+. The value of a is larger for Rb+ than for K+, while the values of n are similar; the activation produced by a given [Rb+]o is larger than that by an equal [K+]o for concentrations less than about 40 mM. Adding a small amount of Rb+ to a K+-containing solution has effects on K+ efflux which depend on [K+]o. At low [K+]o, adding Rb+ increases K+ efflux, the effect being greatest near [K+]o = 30 mM and declining at higher [K+]o; at [K+]o above 40 mM, addition of Rb+ decreases K+ efflux. At [K+]o above 75 mM, where K+ efflux is largely activated, Rb+ reduces K+ efflux by a factor b, described by the relation b = 1/(1+c[Rb+]o). Activation is discussed in terms of binding to at least two sites in the membrane, and the reduction in K+ efflux by Rb+ at high [K+]o in terms of association with an additional inhibitory site.

Animals↗
PubMed1984

Influence of surface charge and transmembrane potential on rubidium-86 efflux of human red blood cells.

The dependence of the rate constant of Rb+ efflux on extracellular cation concentration was measured. At low ionic strengths Rb+ efflux increased strongly. Permeability coefficients were calculated from the rate constants measured, using the Goldman flux equation, with and without making allowance for surface potentials. Only when allowance was made for surface potentials and the associated differences between ion concentrations in the bulk solutions and at the membrane surface, the permeability coefficient remained constant. Best agreement between experimental data and theoretically calculated values was obtained when an interior surface potential of -110 mV was assumed. When the surface charge of erythrocytes is reduced by neuraminidase, the rate constants for Rb+ efflux decreased, indicating a significant influence of surface potential.

Chlorides↗