Rural trauma. Systems in evolution.
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Humans↗
Biomedical subjects
K M Flowe
Publications and source records attributed to K M Flowe.
Gastrin-releasing peptide stimulation of amylase release from rat pancreatic lobules involves intrapancreatic neurons.
Gastrin releasing peptide (GRP) immunoreactivity has been localized to nerve fibers innervating pancreatic acini and identified in nerve cell bodies within intrapancreatic ganglia. The role of intrapancreatic neurotransmission in GRP- and neuromedin C (NmC)-stimulated amylase release was investigated using rat pancreatic lobules in vitro. Lobule responsiveness to neuronal depolarization was demonstrated by amylase release upon exposure to 55 mM potassium (207 +/- 7% of control) or veratridine (294 +/- 12%). Both GRP and NmC produced dose-dependent increases in lobular amylase release, with ED50 values of 1.1 nM and 0.13 nM, respectively. Amylase release in response to submaximal concentrations of GRP were significantly inhibited by tetrodotoxin (78 +/- 5% of control) or hexamethonium (71 +/- 5% of control). GRP-stimulated amylase release was decreased to 71 +/- 5% of control by atropine coincubation. NmC-stimulated amylase release was not affected by tetrodotoxin, hexamethonium, or atropine. GRP (10(-10) to 10(-6) M) produced dose-dependent increments in [3H]acetylcholine release from pancreatic lobules. GRP stimulates amylase release from rat pancreatic lobules by a neurally mediated mechanism in addition to direct action on acinar membrane receptors.
Acetylcholine↗
Galanin inhibits rat pancreatic amylase release via cholinergic suppression.
The effects of galanin on pancreatic exocrine function were examined using rat pancreatic tissues. In anesthetized rats, galanin (40 micrograms/kg/h) decreased amylase secretion stimulated by 2-deoxy glucose (5.8 +/- 0.1 vs. 3.1 +/- 0.1 times basal) and cholecystokinin octapeptide (21.5 +/- 0.6 vs. 16.8 +/- 0.5), while not inhibiting bethanechol-stimulated secretion. In dispersed acini, there was no effect of galanin alone (10(-8) to 10(-13) M) on amylase release, nor did galanin (10(-6) or 10(-8) M) coincubation affect amylase release stimulated by bethanechol (10(-3) to 10(-7) M) or CCK-8 (10(-8) to 10(-13) M). Using pancreatic lobules, coincubation with galanin (10(-6) M) suppressed 75 mM KCl-stimulated amylase secretion and ACh release (10.1 +/- 0.6% vs. 7.3 +/- 0.4%). Veratridine-stimulated (10(-4) M) amylase secretion and ACh release (12.4 +/- 1.7% vs. 8.5 +/- 0.7%) were similarly diminished.
Acetylcholine↗