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Biomedical subjects

K Uvnäs-Wallensten

Publications and source records attributed to K Uvnäs-Wallensten.

At least 19 recordsLinked to original sources
PubMed1982

Reflex activation of the sympatho-adrenal system inhibits the gastrin release caused by electrical vagal stimulation in cats.

The present study on anesthetized cats was performed to investigate how vagally induced gastrin release is influenced by simultaneous activation of the sympatho-adrenal system. The gastrin concentration in portal blood and in antral perfusates was measured with radioimmunoassay. The vagi were activated electrically and the sympatho-adrenal system by bilateral clamping of the carotid arteries. It was found that the vagally induced release of gastrin both into the circulation and into the antral lumen, was markedly inhibited (30% of control values) by simultaneous sympathetic activation, both at neutral and at acid intraantral pH. Infusions of adrenaline or noradrenaline did not mimick the effect on gastrin release induced by clamping of the carotid arteries. It is possible that the inhibitory effect of sympathetic activation on stimulated gastrin secretion is mediated via release of an inhibitory peptide, e.g. somatostatin, from the splanchnic nerves.

Animals↗
PubMed1981

The occurrence of gastrin-17 in the heart.

Radioimmunoassay revealed gastrin-like immunoreactivity in extracts of the heart muscle from cat, guinea pig, rabbit and hog. The immunoreactivity was unevenly distributed, the highest levels being observed in extracts from the atria of the cat heart: in the right atrium approximately 1,000 pg/g or 450 pmol/kg and in the left atrium approximately 4,400 pg/g or 2,000 pmol/kg. In extracts from the cat atria the gastrin-like immunoreactivity was identified as Gastrin-17. The preponderant localization of gastrin to the atria is suggested to be due to the distribution of gastrin containing vagal fibres and nerve terminals in that area, even if a possible localization to specific receptors, Purkinje fibres etc. cannot be excluded. A modulating action on the vagal influence on the heart, either on neurotransmission or on the receptor level, or a direct (perhaps trophic) effect on biochemical processes in the muscle are suggested as possible biological functions of the heart gastrin.

Animals↗
PubMed1981

Effect of apomorphine on peripheral venous gastrin and insulin levels in conscious dogs.

Apomorphine 0.001, 0.005, 0.05 and 0.1 mg/kg were given i.v. to conscious dogs and gastrin and insulin levels were measured in peripheral venous blood. The lowest dose of apomorphine (0.01 mg/kg) did not change gastrin levels but some times caused a decrease of insulin levels, whereas the higher doses (0.005-0.1 mg/kg) induced a dose dependent increase of both hormone levels. The peak shaped release responses appeared within a few minutes and the basal values were reached again within 20 to 30 min. Apomorphine within the dose range which induced a response of insulin and gastrin also caused nausea and vomiting. After pretreatment with haloperidol (0.1 mg/kg) no signs of sickness were observed and the response of gastrin to 0.01 and 0.05 mg/kg of apomorphine was almost completely blocked, whereas the insulin response to both these dose was inhibited to approximately 50%. We conclude that the release of gastrin and insulin can be activated by stimulation of dopaminergic receptors, the anatomical location of which is not clear. Possible sites for the dopaminergic receptors are the hypothalamic region or the vagal centres in the medulla oblongata.

Animals↗
PubMed1981

Effects of apomorphine and haloperidol on plasma cortisol levels in conscious dogs.

Cortisol levels were measured in peripheral plasma of conscious dogs after i.v. administration of apomorphine, a dopaminergic agonist, haloperidol, a dopaminergic antagonist, or apomorphine in combination with haloperidol. Apomorphine in a dose of 0.001 and 0.005 mg/kg did not cause any release of cortisol whereas 0.01 and 0.05 mg/kg caused a dose dependent and peakshaped increase of plasma cortisol levels from 20 to 30 and from 20 to 60 ng/ml respectively. Basal levels were reached again within 1 h. Haloperidol (0.1 mg/kg), when given alone, induced a continuous rise of plasma cortisol levels. After 60 min the levels were approximately 80 ng/ml and still tended to rise. If apomorphine (0.01 mg/kg) was given 30 min after the injection of haloperidol (0.5 mg/kg) no further effect of the apomorphine injections was observed. We therefore speculate that apomorphine activates central dopaminergic receptors which cause a release of ACTH from the pituitary into the circulation, which in turn stimulates the release of cortisol from the adrenals. The fact that not only apomorphine but also haloperidol stimulated cortisol release suggests a complex role or dopamine transmission involving different dopaminergic pathways as well as different dopamine receptors. It is also possible that injection of haloperidol induces a stress reaction in the dogs, which causes a release of cortisol from the adrenals.

Animals↗
PubMed1981

The role of catecholamines in the control of gastrin and acid secretion during insulin hypoglycaemia in man.

5 adrenalectomized subjects and 8 healthy volunteers underwent an insulin test during which acid secretion and plasma adrenaline, noradrenaline, dopamine and gastrin concentrations were measured. Plasma glucose concentration fell by greater than 50% in all subjects. The mean plasma adrenaline concentration increased markedly (greater than 1,000%) in the normal group but was unchanged in the adrenalectomized group. In all subjects, plasma noradrenaline concentration increased moderately, whereas plasma dopamine levels remained unchanged. Clear-cut increments in plasma gastrin concentration were seen only on 3 participants, each of whom responded to insulin hypoglycaemia with an extremely high adrenaline release. Basal and peak acid output were similar in adrenalectomized and normal subjects. The results suggest that circulating catecholamines contribute to the control of gastrin and acid secretion in man only during circumstances with high plasma catecholamine levels, e.g. severe stress.

Adult↗
PubMed1981

Effects of graded doses of somatostatin on gallbladder emptying and pancreatic enzyme output after oral glucose in man.

Effects of intravenous somatostatin on the secretion, motility and absorption in the upper gastrointestinal tract after 75 g oral glucose were examined in healthy subjects with a quantitative multiple indicator dilution method. This report deals with the effects on the gallbladder emptying and the pancreatic enzyme output. Intake of a hypertonic glucose solution induces rapid gallbladder emptying. After early peaks, both biliary and pancreatic enzyme outputs remain at a steady lower level to the end. Somatostatin, started 20 min before the oral load, inhibited dose-dependently the gallbladder emptying and pancreatic enzyme secretion. A maximal inhibition was attained by 1.5 microgram . min-1, and 0.05 microgram . min-1 somatostatin gave a significant 40% reduction. The inhibition persisted in the postinfusion period and was followed by delayed rebound outputs. The gallbladder emptying was completely arrested for variable periods of time, but the pancreatic enzyme secretion was never totally blocked. The promptly established arrest of the gallbladder differed from the slowly initiated inhibition of the gastric and intestinal propulsion. It is proposed that the multiple ways of action of somatostatin and different stimulatory levels contribute to the discrepancies. The study shows that somatostatin induces dose-dependent, long-lasting inhibitions of the biliary and pancreatic responses to oral glucose. The minimal effective dose was a hundred times lower than the dose tested in previous studies in man.

Administration, Oral↗
PubMed1981

Peptides in metabolic autonomic nerves.

Most polypeptides originally assigned to a specific organ and a specific effect seem to occur in many different part of the body, in neurons as well as in endocrine cells. Thus gastrin and insulin, or very similar peptides can be demonstrated in extracts of the vagal nerves and of peripheral somatic nerves. Electrical stimulation of the sciatic nerve of a perfused cat leg causes appearance of gastrin and insulin like immunoreactivity in the perfusates. This gastrin and insulin like immunoreactivity might originate from nervous depots. If so it might be assumed that insulin and other peptides are released in response to activation of autonomic or somatic nerves and that they might exert local metabolic effects in response to the acute needs of energy in eg. striated or smooth muscles.

Animals↗
PubMed1980

Sulphonylurea (glubenclamide) enhances somatostatin and inhibits glucagon release induced by arginine.

Arginine significantly stimulated the release of insulin, glucagon and somatostatin from the isolated perfused rat pancreas. A sulphonylurea, glibenclamide, markedly enhanced the effect of arginine on somatostatin release and inhibited its effect on glucagon release. Insulin release was not modulated by addition of glibenclamide. These findings support the idea of a paracrine interaction of islets hormones.

Animals↗
PubMed1980

Release of gastrin and somatostatin into the gastric lumen of healthy subjects and patients with duodenal ulcer and achlorhydria.

Gastrin and somatostatin were measured in alkaline gastric instillates in normal subjects, patients with duodenal ulcer disease in quiescent state and in patients with achlorhydria. Both peptides were released into the lumen. The gastrin-somatostatin ratio (G/S) in healthy subjects was approximately three. Duodenal ulcer patients had significantly lower G/S ratio due to lower gastrin and higher somatostatin levels whereas in patients with achlorhydria, the G/S ratio did not differ from normal subjects.

Achlorhydria↗
PubMed1980

Decreased release of somatostatin into the portal vein following electrical vagal stimulation in the cat.

Electrical vagal stimulations were performed in anesthetized cats, in which the spleen and the intestine below the duodenum had been removed. The cats were provided with acute antral pouches which were perfused during the experiments. Insulin, glucagon, gastrin and somatostatin were measured in portal vein blood (consisting of blood from the stomach and the pancreas). The antral perfusates were analyzed for gastrin and somatostatin. Electrical vagal stimulation increased the release of insulin and glucagon into the portal vein. Gastrin was elevated in antral perfusates and portal vein blood, whereas somatostatin increased the antral perfusates, but was reduced in portal vein blood. We assume that antral somatotostatin, like gastrin, is released into the blood. The finding that portal vein somatostatin was decreased following vagal stimulation, indicates that the release of somatostatin from another large source of somatostatin, presumably the fundic region of the stomach or the pancreas, was decreased by vagal activation.

Animals↗
PubMed1980

Effect of intraluminal pH on the release of somatostatin and gastrin into antral, bulbar and ileal pouches of conscious dogs.

Experiments were performed on conscious dogs with chronic pouches of the antrum, the duodenal bulb or the ileum, which were perfused with solutions of varying pH. Gastrin and somatostatin levels were measured in the perfusates. When the pouches were perfused with 0.15 M NaCl only small amounts of gastrin and somatostatin (1 pmol/min) were released into the lumen of the antrum and of the duodenal bulb. By lowering pH of the perfusion fluid a pH dependent release of somatostatin was induced into the lumen of the antrum and the duodenal bulb. Perfusion with 0.1 M HCl caused a large output of somatostatin (6--60 pmol/min) into the pouches. The upper pH limit for stimulation of the intraantral or intrabulbar somatostatin release appeared to be approximately pH 3--4. Somatostatin was also released into ileal perfusates at intraluminal pHs below 3--4. Lowering of pH in the antral pouches caused an increased intraluminal gastrin release, which was quantitatively less impressive than that of somatostatin. Occasionally also the gastrin release into the duodenal bulb increased during perfusion with 0.1 M HCl, whereas no such release was induced by acidification of the lumen of the ileum. It is suggested that the inhibition of gastrin release observed at low intraantral pH is mediated by a local effect of somatostatin, since this peptide is released in a pH dependent manner in the antropyloric region. It is also suggested that acidification of any region of the gastrointestinal tract will stimulate the release of peptides from all endocrine cells of the open type, probably by an unspecific effect on the membrane. Thus both gastrin and somatostatin are released by acidification of the antrum, but in the presence of high local levels of somatostatin, the release of gastrin is substantially inhibited.

Animals↗
PubMed1979

Effect of glucose/sulfonylurea interaction on release of insulin, glucagon, and somatostatin from isolated perfused rat pancreas.

The effect of a sulfonylurea, glibenclamide, on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. At glucose concentrations of 1.1 mM or less, the drug stimulated somatostatin release, whereas glucagon release, after 2-3 min of increase, was markedly inhibited. Insulin release was moderately stimulated, and maximal release occurred relatively late. A moderate glucose load (6.7 mM) inhibited glibenclamide-induced release of somatostatin, whereas the two in combination exerted an additive action on insulin release. Greater glucose loads, which by themselves would stimulate somatostatin release, only marginally suppressed glibenclamide-induced somatostatin release. The insulinogenic effect of these glucose levels was not modified by glibenclamide. Glibenclamide may thus stimulate both the alpha and beta as well as delta cells of the pancreas, depending on glucose concentration. We suggest a paracrine (local) interaction of somatostatin with the alpha and beta cells, which has an important role in the kinetics of insulin and glucagon release induced by sulfonylureas.

Animals↗
PubMed1979

Release of gastrin from the skeletal muscles and from the antral mucosa in cats induced by sulfonuric drugs.

The present observations indicate that sulfonuric drugs release gastrin both from peripheral nerves in striated muscles and from endocrine-like cells in the gastrointestinal tract. Gastrin appears in perfusates of extirpated cat legs after administration of tolbutamide or glibenclamide (5-50 mg/kg or 5-500 microgram/kg perfused tissue respectively) to the perfusion medium. Furthermore gastrin is released into the portal vein of cats after i.v. administration of glibenclamide (5-50 microgram/kg). The finding that sulfonuric drugs not only release insulin from beta-cells in the pancreas, but also gastrin from gastrin producing cells in the stomach as well as from nerve fibers in the skeletal muscles, indicate that sulfonuric drugs have more wide spread effects than previously assumed. Possible consequences of the drug induced release of peptides from peripheral nerves as well as of the release of gastrin from the gastrointestinal tract are discussed.

Animals↗