Activation of Na channels in islet cells: metabolic and secretory effects.

Pace, Caroline S.

doi:10.1152/ajpendo.1979.237.2.e130

Cited by 18 publications

(24 citation statements)

References 27 publications

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“…T: gest that possible inhibitory effect Na + K + ATPase, which would pron lation in the beta cell, are overshado modified by other events; that Na passive role in acutely affecting gluc4 hormonal secretion (37,38). This pos ened by recent, detailed studies of m channels by Pace (39 . 4.…”

Section: Discussionmentioning

confidence: 85%

Fluctuations of calcium, phosphorus, sodium, potassium, and chlorine in single alpha and beta cells during glucose perifusion of rat islets.

Kalkhoff¹,

Siegesmund²

1981

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 85%

Fluctuations of calcium, phosphorus, sodium, potassium, and chlorine in single alpha and beta cells during glucose perifusion of rat islets.

Kalkhoff¹,

Siegesmund²

1981

J. Clin. Invest.

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“…The late stimulatory effect was prominent at low and intermediate glucose, but did not occur at high glucose concentrations. Others have found that at nonstimulatory glucose concentrations ouabain either stimulated insulin release (27)(28)(29)(30)(31) or did not affect it (32,33) and no effects were seen with high glucose concentrations (27,(29)(30)(31).…”

Section: Resultsmentioning

confidence: 99%

Evidence for the Involvement of Na/Ca Exchange in Glucose-induced Insulin Release from Rat Pancreatic Islets

Siegel¹,

Wollheim²,

Renold³

et al. 1980

J. Clin. Invest.

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A B S T R A C T Glucose-induced inhibition of Ca++extrusion from the j8-cell may contribute to the rise in cytosol Ca++ that leads to insulin release. To study whether interference with Na/Ca exchange is involved in this inhibition the effects of glucose were compared to those of ouabain. This substance inhibits Na/K ATPase, decreases the transmembrane Na+ gradient in islets, and thus interferes with Na/Ca exchange. Collagenase isolated rat islets were maintained for 2 d in tissue culture with a trace amount of 45Ca++. Insulin release and 45Ca++ efflux were then measured during perifusion. In Ca++-deprived. medium (to avoid changes in tissue specific radioactivity) 16.7 mM glucose inhibited 45Ca++ efflux. Initially 1 mM ouabain inhibited 45Ca++ efflux in a similar fashion, the onset being even faster than that of glucose. The effects of 16.7 mM glucose and ouabain were not additive, indicating that both substances may interfere with Na/Ca exchange. In the presence of Ca++, 16.7 mM glucose induced biphasic insulin release. Ouabain alone caused a gradual increase of insulin release. Again, the effects of ouabain and 16.7 mM glucose were not additive. In contrast, at a submaximal glucose concentration (7 mM) ouabain enhanced both phases of release. An important role for Na/Ca exchange is suggested from experiments in which Ca++ was removed at the time of glucose-stimulation (16.7 mM). The resulting marked inhibition of insulin release was completely overcome during first phase by ouabain added at the time of Ca++ removal; second phase was restored to 60%. This could be due to the rapid inhibitory action ofouabain on Ca++ efflux thereby preventing loss of cellular calcium critical

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“…Veratridine would therefore be expected to depolarize electrically active secretary cells, and this has been observed in islet cells (Pace, 1979). Veratridine also stimulates the release of insulin (Donatsch, Lowe, Richardson & Taylor, 1977;Pace, 1979), posterior pituitary hormones (Nordmann & Dyball, 1979) and catecholamines (Ito, Nakazato & Ohga, 1979), and this has been attributed to increased calcium entry following membrane depolarization. There is some evidence that the electrical activity of the anterior pituitary is modified by agents thought to be responsible for the physiological regulation of hormone release.…”

Section: Introductionmentioning

confidence: 99%

Inhibition by somatostatin of bovine growth hormone secretion following sodium channel activation.

Bicknell¹,

Schofield²

1981

The Journal of Physiology

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SUMMARY1. Growth hormone secretion, exchangeable cellular sodium and calcium concentrations measured by 22Na and 455Ca incorporation, and efflux of 45Ca were studied in dispersed bovine anterior pituitary cells.2. Addition of veratridine (100 /M), an activator of sodium channels, increased exchangeable sodium and calcium concentrations in the cells, the efflux of 45Ca from prelabelled cells, and caused a biphasic stimulation of the rate of growth hormone secretion. Secretion of growth hormone was not stimulated when the extracellular calcium was decreased below 0.1 mM.3. The increases in growth hormone secretion, exchangeable calcium concentration and 45Ca efflux from prelabelled cells caused by veratridine were abolished by addition of the calcium antagonist verapamil (20,uM). Verapamil also reduced the rise in exchangeable sodium caused by veratridine and increased the resting exchangeable sodium concentrations.4. The peptide somatostatin (1 jg/ml) prevented veratridine-stimulated growth hormone secretion but did not inhibit the increases in exchangeable sodium and calcium caused by veratridine. The peptide itself elicited a transient increase in 45Ca efflux and subsequently partially inhibited veratridine-stimulated 45Ca efflux.5. The data suggest that anterior pituitary cells possess voltage-sensitive sodium channels. Activation of these channels by veratridine may lead to depolarization and increased entry of calcium via potential-dependent calcium channels, which contributes to a rise in cytoplasmic calcium concentration and the subsequent stimulation of growth hormone secretion. We conclude that the calcium antagonist verapamil may also interact with sodium channels, and that the peptide somatostatin may act on growth-hormone-secreting cells either to prevent the rise in cytoplasmic calcium by hyperpolarizing the cells or to decrease the affinity of a population of calcium binding sites in the cells.

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Activation of Na channels in islet cells: metabolic and secretory effects.

Cited by 18 publications

References 27 publications

Fluctuations of calcium, phosphorus, sodium, potassium, and chlorine in single alpha and beta cells during glucose perifusion of rat islets.

Fluctuations of calcium, phosphorus, sodium, potassium, and chlorine in single alpha and beta cells during glucose perifusion of rat islets.

Evidence for the Involvement of Na/Ca Exchange in Glucose-induced Insulin Release from Rat Pancreatic Islets

Inhibition by somatostatin of bovine growth hormone secretion following sodium channel activation.

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