Possible role of cytosolic calcium and Na-Ca exchange in regulation of transepithelial sodium transport

Taylor, Ann; Windhager, Erich E.

doi:10.1152/ajprenal.1979.236.6.f505

Cited by 150 publications

(130 citation statements)

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“…It was unlikely that the increased calcium excretion was due to blockade of renal nerve activity as similar responses were recorded in both renally innervated and denervated animals. However, a number of possibilities could account for these responses; firstly, these compounds could block the movement of calcium ions from the tubular fluid into the cells; secondly, they could interfere with the calcium ATPase system at the tubular cells (Katz, 1986); thirdly, they could act indirectly via changes in sodium reabsorption which appears to provide, in part, the energy required to operate the sodium/calcium counter transport system (Taylor & Windhager, 1979).…”

Section: Discussionmentioning

confidence: 99%

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Johns

Manitius

1986

British J Pharmacology

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1In pentobarbitone-anaesthetized rats, intravenous administration of diltiazem at 5 g kg-' min -' did not change blood pressure or renal blood flow but increased glomerular filtration rate by approximately 16%, urine flow by 85%, calcium excretion by 151% and absolute and fractional sodium excretions by 100% and 69%, respectively. A similar pattern of responses was obtained in renally denervated animals, except that calcium excretion did not change statistically. Diltiazem given at 20 pg kg'1 min-' into renally innervated and denervated groups of animals depressed blood pressure between 15-17 mmHg but had no effect on renal haemodynamic or tubular function. 2 Nitrendipine administered at 0.5 ig kg-' min-' to renally innervated and denervated animals significantly depressed blood pressure in intact animals by 6 mmHg and in both groups did not change renal haemodynamics but caused similar increases in urine flow ofbetween 79-98%, calcium excretion of between 87 and 125%, absolute sodium excretion of between 108 and 140% and fractional sodium excretion of between 83 and 170%. Infusion of nitrendipine at 1.0 jig kg-' min' into intact or renally denervated animals decreased blood pressure by 18-20 mmHg and increased urine flow by 84-111 %, calcium excretion by 85%, absolute sodium excretion by 81-137% and fractional sodium excretion by 52-102%. 3 Stimulation of the renal nerves at low frequencies (0.8 to 1.5 Hz) caused minimal changes in renal haemodynamics but decreased urine flow by 27%, calcium excretion by 35%, absolute and fractional sodium excretions 32% and 36%, respectively. In different groups of animals given either diltiazem at 20 pg kg-I min' or nitrendipine at 0.5 pg kg'-min' or 1.0 fg kg'-min' , a similar degree of renal nerve stimulation caused an identical pattern of excretory responses of similar magnitude to those obtained in the absence of drug. 4 The calciuretic, diuretic and natriuretic activities of diltiazem and nitrendipine were not dependent on renal nerves and probably represented a direct action on the tubular reabsorptive processes of these ions. The renal nerve-induced increases in tubular calcium and sodium reabsorption indicate that these a-adrenoceptor-mediated responses are not dependent on the inward movement of calcium

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Section: Discussionmentioning

confidence: 99%

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Johns

Manitius

1986

British J Pharmacology

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“…Whether Na+ is the direct effector for a decrease in apical membrane Na+ permeability or another mediator such as Ca remains to be resolved (cf. Taylor & Windhager (1979)). …”

Section: Apical Selectivitymentioning

confidence: 99%

Apical membrane permeability and kinetic properties of the sodium pump in rabbit urinary bladder.

Lewis¹,

Wills²

1983

The Journal of Physiology

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SUMMARY1. Previous studies have shown that aldosterone stimulates the rate of Na+ transport across the rabbit urinary bladder epithelium by increasing the apical membrane permeability to Na+. Paradoxically, ion-sensitive and conventional micro-electrode measurements demonstrated that intracellular Na+ activity aNa+ was essentially unchanged by aldosterone, i.e. aka+ was constant regardless of the rate of Na+ transport. The present study was designed to resolve this apparent contradiction.2. The effects of elevated, endogenous aldosterone levels produced by low-Na+ diet (Lewis & Diamond, 1976) on urinary bladder Na+ transport were investigated in vitro using Ussing-type chambers and intracellular conventional and ion-sensitive microelectrodes. Apical membrane selectivity and the kinetics of the Na+ pump were assessed as a function of hormone stimulation.3. The aldosterone-stimulated increase in Na+ transport was accounted for by increases in both the relative selective permeability of the apical membrane to Na+ and an increase in its absolute Na+ permeability.4. The kinetics of the Na+ pump were evaluated electrically by loading the cells with Na+ (monitored with Na+-sensitive micro-electrodes) or alternatively by manipulating serosal solution K+ concentration and measuring changes in the basolateral membrane electromotive forces and resistance. From these measurements the current generated by the pump was calculated as a function of intracellular Na+ or extracellular K+. The kinetics of the pump were not altered by aldosterone. A model of highly co-operative binding estimated Km for Na+ as 14-2 mm and 2-3 mm for K+. Hill coefficients for these ions were 2-8 and 1-8, respectively, consistent with a pump stoichiometry of 3 Na+ to 2 K+. The kinetic properties of the Na-K pump indicate that physiological levels of aka+ are poised at the foot of a step kinetic curve which energetically favours Na+ extrusion.

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“…Eliminating the Na+ gradient could be expected to alter intracellular Ca2+ levels and possibly alter intracellular pH (Blaustein & Hodgkin, 1969;Thomas, 1974;Russell & Boron, 1976;Boron et al 1978). Varying Ca2+, in particular, is known to affect membrane resistance (Frankenhaeuser & Hodgkin, 1957) and may affect apical permeability in toad bladder (Taylor, 1980). (3) The change in resistance is not associated with an alteration of Na+ conductance.…”

Section: Permeability Of the Apical Membranementioning

confidence: 99%

Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Eaton¹

1981

The Journal of Physiology

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SUMMARY1. Intracellular potentials and the intracellular activities of Na+ and K+ were examined using conventional and ion-selective micro-electrodes.2. In animals on a normal diet, the intracellular Na+ activity was 8-6 + 2-9 mM (mean + S.D.) with a mean short-circuit current of 2-8 + 09 ,uA/cm2.3. In animals on a low-Na+ diet, the intracellular Na+ activity was 185 + 9-9 mM with a short-circuit current of 4-5+13 ItA/cm2 (mean+ S.D.).4. There was a correlation between short-circuit current and intracellular Na+ activity which could be fitted by a saturating hyperbolic relationship.5. Treatment of the tissue with ouabain and amiloride produced an increase and a decrease, respectively, in the intracellular Na+ activity.6. Treatment with aldosterone produced a large increase in short-circuit current with a substantial increase in intracellular Na+ activity.7. Intracellular Na+ activity does not seem to affect apical membrane permeability directly.

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Possible role of cytosolic calcium and Na-Ca exchange in regulation of transepithelial sodium transport

Cited by 150 publications

References 0 publications

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption

Apical membrane permeability and kinetic properties of the sodium pump in rabbit urinary bladder.

Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

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