Effects of amphotericin B on the electrical properties ofNecturus gallbladder: Intracellular microelectrode studies

Reuss, Luis

doi:10.1007/bf01873340

Cited by 33 publications

(29 citation statements)

References 21 publications

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“…Our results show that blockade after AmB infusion (27 (13,14,30). Exposure to AmB is thus predicted to cause cell depolarization owing to increased sodium influx, an effect which has been demonstrated in skeletal muscle cells (31) and necturus gallbladder cells (32). Depolarization may be followed by increased calcium influx through voltage-gated Ca channels (33).…”

Section: Resultsmentioning

confidence: 52%

Direct vasoconstriction as a possible cause for amphotericin B-induced nephrotoxicity in rats.

Sawaya¹,

Weihprecht²,

Campbell³

et al. 1991

J. Clin. Invest.

105

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In anesthetized rats we tested the hypothesis that amphotericin B (AmB) reduces glomerular filtration rate (GFR) by activating the tubuloglomerular feedback (TGF) mechanism. Infusion of 1 mg/kg AmB over 50 min was followed by a reduction in kidney GFR (from 0.47±0.03 to 039±0.02 ml/min per 100 g body wt during the second hour after infusion; P < 0.05) and by an increase in urine flow and urinary chloride excretion. Singlenephron GFR (SNGFR) measured in proximal (TGF interrupted) or distal tubules (TGF intact) decreased to a similar degree from 33.4±1.8 and 30.6±1.2 nl/min in the control period to 19.7±1.9 and 21.2±1.6 nl/min during the second hour after AmB infusion (P < 0.05). Distal chloride concentrations and TGF responses to changes in loop of Henle flow rate were not significantly altered by AmB. AmB at 10' M reduced the diameter of isolated perfused afferent arterioles from rabbit kidneys. In isometrically contracting rings of rabbit aorta and renal artery in vitro AmB produced endothelium-independent constriction, with half-maximal contraction (ECu,) being achieved by 1.8 X 10' and 2.6 X 10' M in intact vessels and 1.3 X 10-' and 1.7 X 10' M in endothelium-denuded vessels respectively. Tension development did not occur in Ca-free media or in the presence of Ca channel blockers. Pretreatment with ouabain or Bay K 8644 potentiated the effect of AmB. The vasoconstrictive effect of AmB was counteracted by aminophylline and atrial natriuretic peptide. We conclude that the AmBinduced reduction in GFR is not caused by TGF activation and that AmB has a direct vasoconstrictor effect that is probably initiated by depolarization-induced opening of Ca channels. This effect may be an important component of the nephrotoxic actions of AmB. (J. Clin.

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Section: Resultsmentioning

confidence: 52%

Direct vasoconstriction as a possible cause for amphotericin B-induced nephrotoxicity in rats.

Sawaya¹,

Weihprecht²,

Campbell³

et al. 1991

J. Clin. Invest.

105

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“…Potentials and resistances were measured as previously described (Reuss & Finn, 1975a, b;Reuss, 1978). Glass microelectrodes with inner fiber were filled with 3 M KC1 or 4 M K acetate, and sometimes beveled by the technique described by Ogden, Citron and Pierantoni (1978).…”

Section: Electrical Measurementsmentioning

confidence: 99%

Triaminopyrimidinium (TAP+) blocks luminal membrane K conductance inNecturus gallbladder epithelium

Reuss

Grady

1979

J. Membrain Biol.

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The effect of triaminopyrimidinium (TAP+) on the apical membrane of necturus gallbladder epithelial cells was investigated with intracellular microelectrode techniques. TAP+, added to the mucosal bathing solution only, produced the following effects (all rapid and reversible): (i) cell depolarization, (ii) increase of apical membrane resistance, and (iii) decrease of the apical membrane potential change produced by K for Na substitution on the mucosal side. These results can be explained by a decrease of apical membrane K conductance. The paracellular effects of TAP+ were similar to the ones previously described by Moreno (J.H. Moreno, 1974; Nature (London) 251:150; J.H. Moreno, 1975. J. Gen. Physiol. 66:97). These results indicate that the change of transepithelial potential produced by TAP+ cannot be ascribed solely to its effect on the paracellular pathway.

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“…The ionophore itself, in altering the voltage-divider ratio a and Rt may be used as a tool to perform a circuit analysis of the Thevenin equivalents of the epithelium. The technique is similar to that used in the amphotericin B treated rabbit gall-bladder (Cremaschi, Henin, Meyer & Bacciola, 1977;Henin & Cremaschi, 1978), toad urinary bladder (Reuss, Gatzy & Finn, 1978) and in the nystatin treated rabbit urinary bladder (Lewis, Eaton, Clausen & Diamond, 1977;Wills, Lewis & Eaton, 1979 Amphotericin B produces a serosa positive Vt in Necturus gall-bladder (Reuss, 1978), rabbit gall-bladder (Cremaschi etal. 1977) and trout urinary bladder (Fossat & Lahlou, 1982) and several different hypotheses have been advanced to explain the origin of this Vt.…”

Section: Effects Of Amphotericin B On Electrical Parametersmentioning

confidence: 99%

Ion‐selective micro‐electrode studies of the electrochemical potentials in trout urinary bladder.

Harvey¹,

Lahlou²

1986

The Journal of Physiology

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SUMMARY1. Intracellular micro-electtode techniques were used to measure the electrical resistances of the cell membranes and the shunt pathway and intracellular ionic activities in trout urinary bladder when the tissue was incubated in Ringer solution and in the presence of the polyene antibiotic ionophore amphotericin B.2. In control conditions the transepithelial potential was zero and the intracellular potential was -56 mV. The intracellular ionic activities measured with singleand double-barrel ion-sensitive micro-electrodes for the first time in a fish bladder (aka = 16 mm, ak = 87 mm, and a'1 = 21 mM) indicate an active accumulation of K and Cl ions and an active extrusion of Na ions by the cell. The maintenance of intracellular Cl activity above its equilibrium value depended on the presence of Na ions in the mucosal medium, but was independent of the presence of K ions.3. Flat cable analysis yielded values for transepithelial, apical, basolateral and shunt resistances of 197, 2790, 1986 and 205 1 cm-2 respectively. Equivalent circuit analysis using amphotericin B yielded similar values for shunt resistance. The paracellular pathway accounts for 96% of transepithelial current flow and this epithelium may be classified as 'leaky'. The cells are electrically coupled with a space constant of 354 sm.4. Amphotericin B when added to the mucosal solution induced an immediate serosa positive transepithelial potential of about 9 mV and a short-circuit current of 64 1zA cm-2. The Vt was ouabain sensitive and dependent on mucosal Na concentration. The origin of the antibiotic induced transepithelial potential was an increase in the sum of the cell membrane electromotive forces. The apical membrane potential depolarized to -7 mV and its resistance fell to 433 Q cm-2. During the first 10 min ofexposure a'a increased to 80 mm and ak decreased to 7 mm with only a small change in ai1. The changes in cellular Na+ and K+ activities were in accordance with their passive redistribution down their electrochemical gradients. 468 B. J. HARVEY AND B. LAHLOU

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Effects of amphotericin B on the electrical properties ofNecturus gallbladder: Intracellular microelectrode studies

Cited by 33 publications

References 21 publications

Direct vasoconstriction as a possible cause for amphotericin B-induced nephrotoxicity in rats.

Direct vasoconstriction as a possible cause for amphotericin B-induced nephrotoxicity in rats.

Triaminopyrimidinium (TAP+) blocks luminal membrane K conductance inNecturus gallbladder epithelium

Ion‐selective micro‐electrode studies of the electrochemical potentials in trout urinary bladder.

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