Role of calcium in exocrine pancreas secretion VII. Effect of sodium on enzyme secretion and calcium metabolism in rabbit pancreatic fragments and acinar cells

doi:10.1016/0005-2736(81)90349-7

Biochimica et Biophysica Acta (BBA) - Biomembranes

Volume 643, Issue 3, 20 May 1981, Pages 519-534

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Abstract

1.
1. The role of sodium in the pancreatic stimulus-secretion coupling has been studied.
2.
2. Reduction of the extracellular sodium concentration or addition of ouabain to the medium inhibits the stimulation of enzyme secretion by carbachol.
3.
3. Incubation in low sodium medium or in the presence of ouabain increases the exchangeable calcium content, but not the total calcium content of acinar cells.
4.
4. Depending on preincubation time and the substance replacing sodium in the low sodium medium, the carbachol-induced $^{45} · Ca^{2+}$ efflux may be blocked, but it is not blocked by addition of ouabain to a normal Na⁺ medium.
5.
5. Stimulation of enzyme secretion by the calcium ionophore A23187 in the presence of external calcium is inhibited in low sodium as well as in ouabain containing media.
6.
6. These findings suggest that reduction of the Na⁺ gradient across the plasma membrane blocks the coupling between intracellular calcium release and exocytosis, while under certain conditions it also blocks the coupling between hormone-receptor interactions and intracellular calcium release.

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Ouabain- and potassium-induced stimulation of amylase release in fragments and acini of rabbit pancreas
1985, BBA - Molecular Cell Research
Ouabain increases the enzyme secretion from the isolated rabbit pancreas and pancreatic fragments, but not from isolated pancreatic acini. The increase occurs after a delay of 45–60 min and is not accompanied by an increase in lactate dehydrogenase release. The stimulatory effect of ouabain (10⁻⁵ M) is dependent on the presence of extracellular calcium, and is not antagonized by 10⁻⁴ M atropin, 10⁻⁴ M propranolol, 10⁻⁵ M phentolamine, 10⁻³ M dibutyryl-cyclic GMP, 10⁻⁶ M tetrodotoxin, 10⁻⁴ M verapamil or 10⁻⁴ M D-600. Elevation of the extracellular potassium concentration to 120 mM in the presence of 10⁻⁴ M atropin also increases the enzyme secretion from rabbit pancreatic fragments. The increase is again dependent on the presence of extracellular calcium and is resistant to adrenergic blockade and to tetrodotoxin, verapamil or D-600. Forskolin also stimulates a Ca²⁺-dependent release of amylase from pancreatic fragments but not from pancreatic acini. In the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IMX), ouabain (10⁻⁵ M) and K⁺ (120 mM) cause an immediate increase in the cyclic AMP content of pancreatic fragments which does not occur in the absence of extracellular calcium. In pancreatic acini, the cAMP production is only slightly increased by ouabain. In the absence of IMX, the cAMP levels in fragments or acini are not detectably altered by ouabain or K⁺. The results suggest that the stimulation of enzyme secretion by ouabain and high K⁺ is an indirect effect, mediated by the release of an endogenous transmitter from non-cholinergic, non-adrenergic nerves in the intact preparations. The release and/or the effect of the transmitter appears to be mediated primarily by Ca²⁺ and secondarily by cyclic AMP.
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The effect of amiloride on fluid and protein secretion in the isolated rabbit pancreas and on amylase secretion in rabbit pancreatic acini has been studied. Amiloride (1 mM) has no effect on the pancreatic fluid secretion either in a normal incubation medium (143 mM Na⁺), or in a medium containing only 25 mM Na⁺. The carbachol-induced enzyme secretion is inhibited by amiloride in both systems, whereas the enzyme secretion induced by the C-terminal octapeptide of cholecystokinin (PzO) is not affected. Amiloride also inhibits the carbachol-induced ⁴⁵Ca efflux from rabbit pancreatic acini, but again not that induced by PzO. The amiloride concentrations for half-maximal inhibition of carbachol-induced amylase secretion and ⁴⁵Ca efflux are 40 and 80 μM, respectively. Amiloride also competitively inhibits the specific binding of [³H]quinuclidinyl benzylate ([³H]QNB) to rabbit pancreatic acini, suggesting that the amiloride effect is due to competition on the level of the muscarinic acetylcholine receptor.
The actions of tetraethylammonium on dispersed acini from guinea pig pancreas
1983, BBA - Molecular Cell Research
In dispersed acini from guinea pig pancreas, replacing extracellular sodium by tetraethylammonium (1) abolished carbamylcholine-stimulated amylase secretion but did not alter the increase in amylase secretion caused by the C-terminal octapeptide of cholecystokinin, bombesin, ionophore A23187, vasoactive intestinal peptide or 8-bromoadenosine 3′:5′ monophosphate, (2) caused a parallel rightward shift in the dose-response curve for carbamylcholine-stimulated amylase secretion and (3) inhibited binding of $N-[^{3} H]methyl$ scopolamine to muscarinic cholinergic receptors. Detectable inhibition of carbamylcholine-stimulated amylase secretion and binding of $N-[^{3} H]methyl$ scopolamine occurred with 300 μM tetraethylammonium, and half-maximal inhibition of these functions occurred with 1–2 mM tetraethylammonium. Replacing extracellular sodium by Tris did not alter the stimulation of enzyme secretion caused by any secretagogue tested. These results indicate that the tetraethylammonium is a muscarinic cholinergic receptor antagonist and that enzyme secretion from pancreatic acini does not depend on extracellular sodium.
Stimulus-excitation coupling in plasma membranes of pancreatic acinar cells
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Biochimica et Biophysica Acta (BBA) - Biomembranes

Role of calcium in exocrine pancreas secretion VII. Effect of sodium on enzyme secretion and calcium metabolism in rabbit pancreatic fragments and acinar cells

Abstract

Biochim. Biophys. Acta

J. Biol. Chem.

Biochim. Biophys. Acta

J. Biol. Chem.

Biochim. Biophys. Acta

Biochem. Pharmacol.

Biochim. Biophys. Acta

J. Physiol.

J. Clin. Invest.

J. Physiol.

J. Cell. Biol.

J. Cell. Biol.

Am. J. Physiol.

J. Physiol.

J. Physiol.

Am. J. Physiol.

Ouabain- and potassium-induced stimulation of amylase release in fragments and acini of rabbit pancreas

Amiloride is a cholinergic antagonist in the rabbit pancreas

The actions of tetraethylammonium on dispersed acini from guinea pig pancreas

Stimulus-excitation coupling in plasma membranes of pancreatic acinar cells

Cytological effects of ionophore-induced stimulation on the exocrine pancreas of the rat