Mode of stimulation by aldosterone of the sodium efflux in barnacle muscle fibres: effects of ouabain, ethacrynic acid, diphenylhydantoin, (ATPMg)(2‐), adenine translocase inhibitors, pyruvate and oxythiamine.

Bittar, E. Edward; Tallitsch, Robert B.

doi:10.1113/jphysiol.1976.sp011268

Cited by 14 publications

(5 citation statements)

References 28 publications

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“…It is a fact of some importance that cAMP stimulates Na: H exchange and that external pH governs the magnitude of the response of the Na efflux to cAMP. Similar findings have been reported by Bittar & Tallitsch (1976) in connexion with the action of aldosterone on the Na efflux in barnacle fibres. The agreement is not a coincidence but on the contrary significant since the action of aldosterone on the ouabain-insensitive Na efflux is accounted for in terms of increased adenyl cyclase activity.…”

Section: Discussionsupporting

confidence: 90%

“…The agreement is not a coincidence but on the contrary significant since the action of aldosterone on the ouabain-insensitive Na efflux is accounted for in terms of increased adenyl cyclase activity. Thus, one reason for arguing here that the C02-sensitive component of the Na efflux and the ouabain-insensitive Na efflux are one, and the same, is that ethacrynic acid is found to abolish that part of the delayed stimulation caused by aldosterone which is unaffected by ouabain (Bittar & Tallitsch, 1976). The impact of these conclusions is fairly clear.…”

Section: Discussionmentioning

confidence: 71%

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Mode of stimulation by adenosine 3':5'‐cyclic monophosphate of the sodium efflux in barnacle muscle fibres.

Bittar¹,

Chambers²,

Schultz³

1976

The Journal of Physiology

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SUMMARY1. Giant fibres of the barnacle Balanus nubilus have been used as a preparation for studying the mode of action of cAMP on sodium transport.2. It is shown that a concentration of cAMP as low as 106 M, when micro-injected, causes a sharp rise in the radio-Na efflux. Ouabain fails to reverse the cAMP effect.3. The magnitude of the response of the Na efflux to cAMP is markedly reduced by pre-injecting 100 or 500 mM-EGTA solutions or by omitting Ca2+ from the bathing medium. Both together fail to bring about a greater reduction in the response.4. The response to cAMP is greatly reduced by pre-injecting the protein inhibitor of Walsh and practically abolished by pre-injecting 500 mM-EGTA and soaking in Ca-free artificial sea water, ASW.5. The Ca2+-independent component of the Na efflux which is also stimulated by cAMP is shown to involve Na for H exchange. The magnitude of this exchange is governed by external pH. 6. The Na efflux into Ca2+-free, Li+-ASW is shown to be markedly stimulated by injecting cAMP, an effect which is enhanced by reducing external pH.7. The Na efflux at 00 C is stimulated by injecting cAMP. This is shown to be related to activation of the protein kinase by cAMP and to depend on the presence of external Ca2+.8. (i) Ethacrynic acid when injected reduces the ouabain-insensitive Na efflux into HEPES-Ca2+-free ASW at pH 6-3. These same fibres show a marked response to cAMP.(ii) The ouabain-insensitive Na efflux into HCO3 , Ca2 -free ASW from fibres pre-treated with ethacrynic acid fails to respond to external acidification. This is interpreted as indicating that ethacrynic acid inactivates 21 PHY 257 E. E. BITTAR AND OTHERS the C02-sensitive adenyl cyclase system. These same fibres when injected with cAMP show a marked response.(iii) Stimulation of the ouabain-insensitive Na efflux into HCO-, Ca2+-free ASW by external acidification is reversed by injecting ethacrynic acid. These fibres when injected with cAMP show a reduced response.9. It is concluded that: (i) stimulation of the Na efflux by injected cAMP is mainly due to activation of cAMP-dependent protein kinase;(ii) the underlying exchange mechanism consists of Na: Ca and Na: H exchange. Interaction of Ca2+ with a phosphorylated membrane, thereby modifying permeability remains as a real possibility;(iii) the site of action of CO2 and ethacrynic acid is the adenyl cyclase system.10. The implications of activation of the adenyl cyclase system by CO2 and Na: H exchange are briefly touched upon.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 71%

Mode of stimulation by adenosine 3':5'‐cyclic monophosphate of the sodium efflux in barnacle muscle fibres.

Bittar¹,

Chambers²,

Schultz³

1976

The Journal of Physiology

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“…The relevant clinical situation was imitated in the present study by treating dogs (group 1) with diuretics to induce hypokalemia. A second group was treated with mineralocorticoid to mimic a hyperaldosteronic condition since, in contrast to digitalis, mineralocortocoids stimulate membrane Na+-K+ ATPase (Bittar & Tallitsch, 1976) resulting in an increased potassium concentration in groups 1 and 2 (interaction between digoxin and mineralocorticoid).…”

Section: Discussionmentioning

confidence: 99%

Digoxin Toxicity Compared With Myocardial Digoxin and Potassium Concentration

Steiness¹

1978

British J Pharmacology

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1 Twenty-nine dogs were given digoxin (0.25 mg) by mouth twice daily for eight days. Some of them (group 1) also received diuretics and others (group 2) a mineralocorticoid. The dogs were then given an intravenous bolus injection of digoxin and plasma and cardiac muscle were analysed for digoxin and potassium. 2 In the digitalized dogs, myocardial potassium concentration decreased following the intravenous injection of either 0.05 or 0.15 mg/kg digoxin; in contrast, in those dogs given diuretics or mineralocorticoid the potassium concentration increased. 3 Ventricular arrhythmias occurred after digoxin injection (0.05 mg/kg) in the hypokalemic dogs, in those given a mineralocortocoid and in those dogs which received a toxic digoxin dose (0.15 mg/kg). No arrhythmias where seen in the control (digitalized) group. 4 Myocardial digoxin concentrations were similar in the control digitalized group and in the mineralocorticoid-treated dogs after the intravenous administration of the lower digoxin dose (0.05 mg/kg). The myocardial digoxin concentration was significantly higher in the hypokalemic group and in the group receiving the higher digoxin dose (0.15 mg/kg). 5 There was no obvious relationship between the occurrence of arrhythmias and the myocardial concentration of digoxin or potassium.

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“…The effect ofethacrynic acid, at concentrations below 10-2 M, on the hydraulic conductivity of the isolated rabbit ciliary epithelium is expected since ouabain has been shown to have no effect on hydraulic conductivity (Green & Mayberry, 1984), although altering the electrical characteristics of the ciliary epithelium (Kishida et al 1981;Krupin et al 1982). Ethacrynic acid is known to inhibit Na+,K+-dependent ATPase in several systems (Burg & Green, 1973;Bittar & Tallitsch, 1976) and, as a consequence, alter the ionic permeability ofmembranes (Danielson, Bittar, Chen & Tong, 1972;Fromter & Gessner, 1975); its action, therefore, would be expected to be similar to that of ouabain in the ciliary epithelium, although different ATPases may be affected by the two drugs. That hydraulic conductivity was unaffected as a consequence of application to the ciliary epithelium may indicate that the pathway for fluid permeability is via a paracellular, not the cellular, pathway, as for ouabain (Green & Mayberry, 1984).…”

Section: Discussionmentioning

confidence: 99%

“…Ethacrynic acid is known to inhibit Na+,K+-dependent ATPase in several systems (Burg & Green, 1973;Bittar & Tallitsch, 1976) and, as a consequence, alter the ionic permeability ofmembranes (Danielson, Bittar, Chen & Tong, 1972;Fromter & Gessner, 1975); its action, therefore, would be expected to be similar to that of ouabain in the ciliary epithelium, although different ATPases may be affected by the two drugs. That hydraulic conductivity was unaffected as a consequence of application to the ciliary epithelium may indicate that the pathway for fluid permeability is via a paracellular, not the cellular, pathway, as for ouabain (Green & Mayberry, 1984).…”

Section: Discussionmentioning

confidence: 99%

Drug Effects on the Hydraulic Conductivity of the Isolated Rabbit Ciliary Epithelium

Green

Mayberry

1985

Exp Physiol

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SUMMARYThree aspects of hydrostatically driven volume flow across the isolated rabbit ciliary epithelium have been examined. (1) Hydraulic conductivity was increased in a dose-dependent manner by amiloride, but not by furosemide, indicating that amiloride may interfere with junctional permeability. The absence of a furosemide effect suggests that regulation of passive fluid movement may be independent of net ionic fluxes of either chloride or bicarbonate. Ethacrynic acid had no effect on hydraulic conductivity at concentrations below 10-2 M. At 10-2 M, hydraulic conductivity was decreased, suggesting that fluid pathways may be linked to ionic pathways. (2) Successive in vivo daily treatments with adrenergic agonists result in changes in the intraocular pressure response. Dose-effect curves to in vitro agonists from eyes pre-treated on successive days indicate that isoprenaline caused a lack of response in hydraulic conductivity after 3 d of in vivo treatment, adrenaline caused responses after 2 d which were about half of those found on day 0, while phenylephrine and noradrenaline had no influence on hydraulic conductivity. These data suggest that ,8-agonists cause a deactivation or desensitization of some moiety which is coupled with regulation of hydraulic conductivity in a manner similar to that seen for the fl-receptor-coupled adenylate cyclase. (3) While cyclic GMP was without effect, various modifiers ofcyclic GMP activity increased hydraulic conductivity. Alteration of cellular cyclic GMP levels appears to exert some regulation over ciliary epithelial permeability.

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Mode of stimulation by aldosterone of the sodium efflux in barnacle muscle fibres: effects of ouabain, ethacrynic acid, diphenylhydantoin, (ATPMg)(2‐), adenine translocase inhibitors, pyruvate and oxythiamine.

Cited by 14 publications

References 28 publications

Mode of stimulation by adenosine 3':5'‐cyclic monophosphate of the sodium efflux in barnacle muscle fibres.

Mode of stimulation by adenosine 3':5'‐cyclic monophosphate of the sodium efflux in barnacle muscle fibres.

Digoxin Toxicity Compared With Myocardial Digoxin and Potassium Concentration

Drug Effects on the Hydraulic Conductivity of the Isolated Rabbit Ciliary Epithelium

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