Aldosterone and insulin effects on driving force of Na+ pump in toad bladder

Siegel, Bernard B.; Civan, MM

doi:10.1152/ajplegacy.1976.230.6.1603

Cited by 46 publications

(20 citation statements)

References 7 publications

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“…6, we propose that insulin is one of perhaps many activators of PKC in frog skin and other tight epithelial cells. This hypothesis is supported by many lines of indirect evidence: (i) insulin stimulates Na § transport across toad urinary bladder (Herrerra, 1965) and short-circuit current across frog skin (Herrerra, Whittembury & Planchart, 1963;Erlij & Schoen, 1981); (ii) this stimulation reflects not only a primary stimulation of the Na,K-exchange pump (Siegel & Civan, 1976), but an enhancement of P~Pa as well (Erlij & Schoen, 1981;Walker et al, 1984;Schoen & Erlij, 1985); (iii) insulin stimulates production of diacylglycerol (DAG) in cultured myocytes by increasing the rate of hydrolysis of a phosphatidylinositol-glycan (PhlG) to DAG and an inositol-phosphate glycan (IPG) (Saltiel et al, 1986); (iv) DAG can be translocated from one plasma membrane to intracellular membranes and presumably to the contralateral plasma membrane (Pagano & Longmuir, 1985); (v) DAG is a physiologic activator of PKC (Kaibuchi et al, 1981) which stimulates Na § transport across frog skin (Table 1 , Fig. 1); and (vi) at least one Na § channel protein seems to be a substrate for PKC (Costa & Catterall, 1984).…”

Section: Discussionmentioning

confidence: 90%

Diacylglycerols stimulate short-circuit current across frog skin by increasing apical Na+ permeability

1987

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The phorbol ester TPA (12-O-tetradecanoylphorbol-13-acetate) stimulates baseline Na+ transport across frog skin epithelium and partially inhibits the natriferic response to vasopressin. The effects are produced largely or solely when TPA is added to the mucosal surface of the tissue. Although TPA activates protein kinase C, it has other effects, as well. Thus, the biochemical basis for the effects and the ionic events involved have been unclear. Furthermore, the physiologic implications have been obscure because of the sidedness of TPA's actions. We now report that two synthetic diacylglycerols (DAG) replicate the stimulatory and inhibitory effects of TPA on frog skin. DAG is the physiologic activator of PKC. In this tissue, it produces half-maximal stimulation at a concentration of less than or equal to 19 microM. In contrast to TPA, DAG is about equally effective from either tissue surface. In a series of eight experiments, DAG was found to depolarize the apical membrane. Diacylglycerol also increases the paracellular conductance of frog skins bathed with mucosal Cl- Ringer's solution. The latter effect can be minimized by replacing NO3- for Cl- in the mucosal solution. Under these conditions, combined intracellular and transepithelial measurements indicated that DAG increased both the apical Na+ permeability and intracellular Na+ concentration. These results are qualitatively similar to the effects of cyclic 3',5'-AMP on this tissue, suggesting that activation of PKC by DAG causes phosphorylation of the same or nearby gating sites phosphorylated by cAMP. We propose that apical Na+ entry is regulated in part by activation of PKC, and that insulin may be a physiologic trigger of this activation.

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Section: Discussionmentioning

confidence: 90%

Diacylglycerols stimulate short-circuit current across frog skin by increasing apical Na+ permeability

1987

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“…In each row, the two sets of records were obtained from the same tissue under the same conditions at approximately the same time. Application of the KolmogorovSmirnov test as previously described (Siegel & Civan, 1976) indicates that the distributuon of the differences between the paired sets of measurements is not significantly different (at the 0.20 probability level) from a t-distribution. Therefore, the Student t-test can be applied; the mean difference in activity of -1.1 mM is thereby found insignificantly different from zero, at the 0.10 probability level.…”

Section: Methodsmentioning

confidence: 88%

Dissociation of cellular K+ accumulation from net Na+ transport by toad urinary bladder

DeLong

Civan

1978

J. Membrain Biol.

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Summary.A number of published data suggest a variable stoichiometry between the rates of cellular potassium uptake and net sodium transport (JNa) across the urinary bladder of the toad. This problem was examined by simultaneously studying the iutracellular chemical activity of potassium (aK) with open-tip K+-selective microelectrodes and micropipets, and monitoring JNa by measuring the short-circuit current (SCC). When bathed in the short-circuited state with solutions containing an a• of 2.7 mrs, the mean + SEM values for intracellular aK were 43 _+ 0.6 m•.Ouabain, at a concentration of 10 -2 M, reduced intracellular aK by 56-67% and SCC by 96-100%. At 5 x 10 .4 M, ouabain reversibly reduced intracellular aK by 40-55%, and SCC by 63-68%; the inhibition of SCC was only partly reversible during the period of observation.Removal of external potassium reduced intracellular aK by 69-80% and SCC by 51-76%. Restoration of external potassium entirely returned intracellular aK to its control value, but only Partially reversed the inhibition of SCC during the period of study. Furthermore, recovery of aK began 19-43rain before that of SCC; recovery of aK was 90-97% complete before any increase in SCC could be measured. Although other interpretations are possible, the simplest interpretation of the data is that the processes responsible for potassium accumulation and transepithelial sodium transport are not identical. We propose the existence of a separate transfer mechanism at the basolateral cell membrane, responsible for accumulating intracellular potassium, and not directly coupled to active sodium transport.

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“…Insulin exerts its natriferic effect on frog skin by at least two mechanisms, a direct stimulation of the Na,K-exchange pump (10,11) and an increase in the apical Na+ permeability (12,13). The intracellular mediators are unknown.…”

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confidence: 99%

Insulin and phorbol ester stimulate conductive Na+ transport through a common pathway.

Civan

Peterson-Yantorno

O’Brien

1988

Proc. Natl. Acad. Sci. U.S.A.

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Insulin stimulates Na+ transport across frog skin, toad urinary bladder, and the distal renal nephron. This stimulation reflects an increase in apical membrane Na+ permeability and a stimulation of the basolateral membrane Na,K-exchange pump. Considerable indirect evidence has suggested that the apical natriferic effect of insulin is mediated by activation of protein kinase C. However, no direct information has been available documenting that insulin and protein kinase C indeed share a common pathway in stimulating Na+ transport across frog skin. In the present work, we have studied the interaction of insulin and phorbol 12-myristate 13-acetate (PMA), a documented activator of protein kinase C. Preincubation of skins with 1,2-dioctanoylglycerol, another activator of protein kinase C, increases baseline Na+ transport and reduces the subsequent natriferic response to PMA. Preincubation with PMA markedly reduces the subsequent natriferic action of insulin. This effect does not appear to primarily reflect PMA-induced internalization of insulin receptors. The insulin receptors are localized on the basolateral surface of frog skin, but the application of PMA to this surface is much less effective than mucosal treatment in reducing the response to insulin. Preincubation with D-sphingosine, an inhibitor of protein kinase C, also reduces the natriferic action of insulin. The current results provide documentation that insulin and protein kinase C share a common pathway in stimulating Na+ transport across frog skin. The data are consistent with the concept that the natriferic effect of insulin on frog skin is, at least in part, mediated by activation of protein kinase C.

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Aldosterone and insulin effects on driving force of Na+ pump in toad bladder

Cited by 46 publications

References 7 publications

Diacylglycerols stimulate short-circuit current across frog skin by increasing apical Na+ permeability

Diacylglycerols stimulate short-circuit current across frog skin by increasing apical Na+ permeability

Dissociation of cellular K+ accumulation from net Na+ transport by toad urinary bladder

Insulin and phorbol ester stimulate conductive Na+ transport through a common pathway.

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