Jørgen Hedemark Poulsen

Partial dissociation between salivary secretion and active potassium transport in the perfused cat submandibular gland.

SummaryIsolated cat submandibular glands were perfused with Locke solutions in a thermostated chamber. Passive loss of potassium and uptake of sodium was achieved either by increasing the permeability of the cell membranes by acetylcholine (ACh) or by inhibiting the sodium-potassium pump reversibly by cooling or by removal of extracellular potassium. Irrespective of the way by which the cells were potassium depleted and sodium loaded, re-establishment of normal conditions was sufficient to cause an active net uptake of potassium (probably coupled to net extrusion of sodium). However, while ACh-induced changes in intracellular concentrations of monovalent cations were accompanied by salivary secretion, virtually no secretion was observed when normal conditions were re-established after concentration changes caused by inhibiting the sodium-potassium pump. It is concluded that while the transport mechanisms responsible for the maintenance of the intracellular concentrations of monovalent cations undoubtedly is a (Na+−K+)-activated ATPase, the transport mechanism responsible for the formation of the primary saliva is probably of a different type, since it apparently is not directly activated by the intracellular sodium concentration.

Peptide-evoked release of amylase from isolated acini of the rat parotid gland

Investigations of the effects of the neuropeptides, substance P (SP), neurokinin A (NKA), neuropeptide K (NPK), gastrin releasing peptide (GRP), calcitonin gene related peptide (CGRP) and vasoactive intestinal peptide (VIP), and of acetylcholine on amylase secretion have been carried out on isolated acini of the rat parotid gland. Furthermore, the occurrence and location of the peptides in the gland was studied. Finally, binding of 125I-BH-SP to isolated acini were studied in order to characterize their tachykinin receptor(s) and their binding kinetics. Only SP, NKA, NPK and VIP stimulated amylase release. VIP, however, with a rather low potency (EC50 at 155 nmol/l). Simultaneous stimulation with two compounds elicited additive responses, except for VIP and acetylcholine which elicited an effect significantly above additive response. Only SP, NKA, VIP and CGRP could be identified in extracts of the gland. The immunoreactivity of these peptides could be located to varicose nerve fibers in the gland. Binding of labeled SP to the isolated acini exhibited the characteristics of a genuine agonist/receptor interaction, and the rank order of displacement potencies indicated the presence of NK1-receptors. Thus, the results of the present study support previous suggestions that the tachykinins and VIP are likely to be involved in amylase secretion in the rat parotid gland.

Time course of acetylcholine-induced K + release from the perfused cat submandibular gland.

SummaryThe cat submandibular gland was perfused at constant pressure either with a standard Locke solution or a Locke solution containing teophylline (5×10−3 M). Stimulation was carried out by close intraarterial injection of a Locke solution containing acetylcholine chloride and131I-labeled rabbit serum albumin as a marker. The acetylcholine-induced increase in venous potassium concentration as well as the venous131I-activity were measured in single-drop samples taken at short intervals (ca. 0.5 s).The time difference between the appearance time of the stimulation marker and the increase in venous potassium concentration was 0.54 s (SE=0.06,n=9) during perfusion with standard Locke solution. During perfusion with Locke solution containing teophylline the time difference was 1.00 s (SE=0.07,n=9).It is concluded that it has not been possible to detect temporal discrepancies between the acetylcholine-induced potassium loss and the hyperpolarization of the acinar cell membrane. This finding is in accordance with the hypothesis of a common cause of the two phenomena, namely diffusion of potassium along its electrochemical gradient from the cells to the perfusion fluid, due to an enhanced membrane permeability evoked by acetylcholine.

Antral Hypergastrinemia – A Report of Three Cases

Three patients with juxtapyloric ulcers and hypergastrinemia are presented. Fasting and food-stimulated serum gastrin concentration (SGC) were measured in 1970, 1972 and 1973 before the primary ulcer operation (selective gastric vagotomy and Jaboulay gastroduodenostomy; SGV + GD). Fasting SGC were 105, 149 and 158 pg/ml and the postprandial concentrations were 400, greater than 800 and greater than 800 pg/ml, respectively. The pentagastrin-stimulated acid secretion was within the normal range. After SGV + GD, only a slight decrease in acid secretion was observed. The hypergastrinemia persisted unchanged or decreased slightly in 1 patient. A recurrent ulcer developed and a precise antrectomy was carried out. Postoperatively, the fasting SGC was markedly reduced and the postprandial gastrin response abolished. The resected specimens were subjected to immunocytochemical gastrin cell quantitation. The number of gastrin cells was elevated in all 3 patients and the gastrin cell topography was distorted, with cells being present both in the lower and upper thirds of the antropyloric glands.

Liberation of acetylcholine by ouabain in the cat submandibular gland

SummaryThe ability of ouabain to initiate loss of potassium and salivary secretion from the perfused cat submandibular gland has been studied in the absence and presence of atropine. Ouabain (10−4 M) when given alone caused a net efflux of potassium amounting to 4.25 μEq×min−1×g−1 and induced salivary secretion. When ouabain was given together with atropine (7.2×10−5 M) the net efflux of potassium was 1.00 μEq×min−1×g−1 while no saliva was secreted.In glands loaded with42K the rate constant of the efflux of42K was increased when the perfusion fluid contained ouabain. When atropine was given before and during administration of ouabain, there was no change in the rate constant.The results indicate that ouabain causes a liberation of acetylcholine, which in turn increases the permeability of the glandular cells to potassium and elicits salivary secretion.