The action of ethacrynic acid on sodium efflux from single toad oocytes

Bittar, E. Edward; Dick, D. A. T.; Fry, D.

doi:10.1113/jphysiol.1968.sp008530

Cited by 27 publications

(10 citation statements)

References 13 publications

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“…This observation has been extended to several types of cells (Bittar, 1966;Bittar, Dick & Fry, 1968; Klahr, Shaw, Hwang & Miller, 1969;Macknight, 1969;Whittembury & Fishman, 1969). We have described briefly (Leblanc & Erlij, 1969) that ethacrynic acid inhibits the sodium-dependent component of sodium efflux in frog striated muscle.…”

Section: Introductionmentioning

confidence: 80%

The effects of ethacrynic acid and other sulphydryl reagents on sodium fluxes in frog muscle

Erlij¹,

Leblanc²

1971

The Journal of Physiology

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1. Ethacrynic acid (2 m M) increased the sodium efflux from freshly dissected frog sartorius muscles. This increase was not observed in muscles previously treated with strophanthidin. 2. In strophanthidin‐treated muscles, the addition of ethacrynic acid (2 m M) caused a reduction of sodium efflux. The value of efflux reached in these muscles is similar to that observed in muscles immersed in sodium‐free solutions containing strophanthidin. 3. Ethacrynic acid reduced sodium influx into strophanthidin‐treated muscles. Potassium influx was not affected by this substance. These findings suggest that the inhibitor blocks an exchange of sodium for sodium. 4. The increase in sodium efflux caused by ethacrynic acid did not result from depolarization nor from an increase in [Na]i. 5. Ethacrynic acid caused only a reduction of sodium efflux in muscles previously loaded with sodium by prolonged immersion in potassium‐free solutions at low temperatures. 6. A derivative of ethacrynic acid that lacks the ability to combine with sulphydryl (SH) groups did not reduce sodium efflux from muscles treated with strophanthidin. 7. Para‐chloromercuribenzoic acid (PCMB) reduced sodium efflux from control and strophanthidin‐treated muscles. This reduction seems to be restricted to the sodium dependent component of the efflux. 8. The inhibition of the sodium‐dependent component of sodium efflux caused by ethacrynic acid and PCMB appears to have a similar mechanism, namely, the combination with SH groups.

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Section: Introductionmentioning

confidence: 80%

The effects of ethacrynic acid and other sulphydryl reagents on sodium fluxes in frog muscle

Erlij¹,

Leblanc²

1971

The Journal of Physiology

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“…DISCUSSION Ethacrynic acid, a potent sulfhydryl inhibitor and diuretic agent in humans (13), has been shown to interfere with active cation transport in renal tubules (14), kidney slices (15,16), toad bladder (17), smooth muscle (18), striated muscle (19), toad oocytes (20), and human erythrocytes (3,4,(20)(21)(22)(23). As such it appears to have widespread inhibitory potency for active cation transport.…”

Section: Resultsmentioning

confidence: 99%

The effects of transport inhibitors on sodium outflux and influx in red blood cells: evidence for exchange diffusion

Dünn¹

1970

J. Clin. Invest.

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A iB S T R A C T Active sodium transport (outflux or efflux) in red blood cells generally has been measured by assessing the amount of outflux inhibited by digitalis glycosides (outflux-fraction I). The presence of a ouabain-uninhibited sodium outflux (outflux-fraction II) attributable either to a second active transport mechanism or to exchange diffusion has been the subject of recent investigations. In the present study a variety of transport inhibitors, including ouabain, ethacrynic acid, furosemide, oligomycin, and amiloride, were studied for their effects on these components of sodium transport in RBC.In the presence of ouabain both ethacrynic acid and furosemide exerted similar effects on sodium outflux, inhibiting approximately 0.5 mmoles/L of cells per hr. This component of sodium outflux has been called outflux-fraction II. Ethacrynic acid showed no inhibitory potency when ouabain and furosemide were present, thereby suggesting that the same outflux component (fraction II) was affected by ethacrynic acid and by furosemide. In addition, furosemide reduced sodium influx to the same extent that it reduced sodium outflux. Outflux-fraction II, as defined by furosemide, did not contribute a net sodium outflux. These results of sodium outflux and influx experiments confirm the existence of a transport pathway which does not contribute to net flux and which fits the definition of exchange diffusion.

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“…Ethacrynic acid interferes with sodium chloride transport in a variety of tissues (24)(25)(26)(27). The inhibitory efaTheophylline indeed inhibits cyclic nucleotide phosphodiesterases, thereby permitting accumulation of intracellular cAMP through basal activity of adenyl cyclase (18,19).…”

Section: Discussionmentioning

confidence: 99%

Effects of Ethacrynic Acid on the Isolated Collecting Tubule

Abramow¹

1974

J. Clin. Invest.

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A B STRACT Effects of the diuretic ethacrynic acid on osmotic water permeability were investigated in the isolated perfused collecting tubule of the rabbit kidney.The base-line water permeability of the collecting tubule was not affected when the drug (10-'M) alone was added to the bathing medium. Vasopressin alone in the bathing medium (2, 5 AU/ml) elicited a significant increase in osmotic water absorption. With vasopressin kept in the bathing medium, the addition of 10-'M ethacrynic acid depressed the hydro-osmotic effect of vasopressin by 50%. This inhibitory effect of low concentrations of ethacrynic acid could be surmounted by high, supramaximal dosage levels of vasopressin.When 10-4M ethacrynic acid was added to the bathing medium before vasopressin, the hydro-osmotic effect of vasopressin and the diuretic in combination was insignificant.Dibutyryl adenosine 3'5'-monophosphate (10-4-10-'M) alone in the bathing medium significantly increased baseline osmotic water flow, mimicing the effect of antidiuretic hormone. When ethacrynic acid was added together with the nucleotide, the permeability remained at the same high level. Theophylline, like the nucleotide and vasopressin, produced a significant hydro-osmotic effect. The magnitude of this responise was not affected by further addition of ethacrynic acid (10-4`\).It was concluded that ethacrynic acid is an antagonist of antidiuretic hormone. The antagonism probably occurs at the level of the receptor site of the hormone on the peritubular membrane. Antagonism to circulating antidiuretic hormone may therefore be one of the factors involved in the loss of renal concentrating ability brought about by ethacrynic acid diuresis.

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The action of ethacrynic acid on sodium efflux from single toad oocytes

Cited by 27 publications

References 13 publications

The effects of ethacrynic acid and other sulphydryl reagents on sodium fluxes in frog muscle

The effects of ethacrynic acid and other sulphydryl reagents on sodium fluxes in frog muscle

The effects of transport inhibitors on sodium outflux and influx in red blood cells: evidence for exchange diffusion

Effects of Ethacrynic Acid on the Isolated Collecting Tubule

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