Calcium‐dependent amylase release and electrophysiological measurements in cells of the pancreas

Abstract

SUMMARY1. Transmembrane potential, effective membraneresistance, and amylase output were recorded from acinar cells of rat pancreas perfused in vitro.2. Both pancreozymin and acetylcholine hyperpolarized the acinar cells, increased effective membrane resistance, and augmented amylase output.3. The omission of calcium from the perfusion medium increased effective membrane resistance and potential, and abolished the increase in amylase output in response to the drugs. 4. A quantitative relation was found between the amount of amylase released by pancreozymin and the concentration of calcium in the perfusion medium at values below the normal 2*5 mm calcium. Excess magnesium did not inhibit the increase in amylase output in response to the drug.5. It is concluded that the release of amylase from the pancreas depends on the entry of calcium into the acinar cells. The entry of calcium seems to be mediated by a carrier in the membrane and may be considered as a 'facilitated diffusion'.6. The electrophysiological findings taken together with morphological evidence provided by scanning electron microscopy favour the view that pancreatic zymogens are released from the granules in the acinar cells to the lumen by the process known as exocytosis.

EFFECT OF ANTI‐INFLAMMATORY DRUGS ON THE MEMBRANE POTENTIAL OF VASCULAR ENDOTHELIAL CELLS in vitro

“…Smooth muscle cells appear to retain their membrane potential in the absence of calcium provided that magnesium ions are present (Bulbring & Tomita, 1970). Certain non-excitable cells actually show a hyperpolarization when extracellular calcium is removed (Kanno, 1972). This latter study, however, was conducted in the continued presence of magnesium.…”

“…Few observations have been made previously of the electrical properties of vascular endothelium. Funaki (1961) (Adrian, 1956;Dean & Matthews, 1970;Kanno, 1972;Okado, Ogawa, Aoki & Izutsu, 1973 Electrically excitable cells usually depolarize in the absence of extracellular calcium (Frank & Inoue, 1973). Smooth muscle cells appear to retain their membrane potential in the absence of calcium provided that magnesium ions are present (Bulbring & Tomita, 1970).…”

“…Anti-inflammatory drugs with a lanthanum-like action included indomethacin, ibuprofen, phenylbutazone and aminopyrine as well as flufenamic, meclofenamic and salicylic acids (Table 2). Phenylacetic acid, which is related to indomethacin chemically but which lacks antiinflammatory activity (Northover, 1964;Durant, Smith, Spickett & Szarvasi, 1965) failed to prevent depolarization (Table 2). However, a number of drugs with well-established anti-inflammatory activity also failed to inhibit heat-induced depolarization.…”

Dynamic analysis of secretagogue-induced amylase secretion from rat pancreatic acini studied by perifusion system.

“…In a calcium free medium containing EGTA or EDTA, CCK or cholinergic agoniststimulated enzyme secretion was abolished in the isolated pancreas (ARDENT et al, 1973 ;KANNO, 1972), pancreatic slices (HOKIN, 1966) and fragments (BENZ et al, 1972;CASE and CLAUSEN, 1973), or decreased in pancreatic fragments (HEISLER et al, 1972;ROBBERECHT and CHRISTOPHE, 1971). Some investigators found that the initial secretion evoked by cholinergic agents of CCK was not affected yet the subsequent secretion was decreased or absent in the calcium free solution containing EGTA, in cases of the isolated pancreas (SCHREURS et al, 1976), pancreatic segments (PETERSEN and VEDA, 1976), lobules (SCHEELE and HAYMOVITS, 1979), dispersed acinar cells (SCHULZ et al, 1981), and acini .…”

“…Many investigators previously demonstrated the requirement of extracellular calcium for CCK or cholinergic agents-induced enzyme secretion (ARGENT et al, 1973;BENZ et al, 1972;CASE and CLAUSEN, 1973;HEISLER et al, 1972;HOKIN, 1966;KANNO, 1972;KANNO and NISHIMURA, 1976;ROBBERECHT and CHRISTOPHE, 1971). Some investigators proposed the hypothesis that the triggering of stimulation is independent of extracellular calcium but is dependent on calcium from intracellular stores PETERSEN and VEDA, 1976;SCHEELE andHAYMOVITS, 1979: SCHULZ et al, 1981).…”