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Biomedical subjects

K Hermansen

Publications and source records attributed to K Hermansen.

At least 145 records · Page 8Linked to original sources
PubMed1979

Differential sensitivity to somatostatin of pancreatic polypeptide, glucagon and insulin secretion from the isolated perfused canine pancreas.

This dose-response study deals with the relative inhibitory effect of somatostatin on the acetylcholine-stimulated release of pancreatic polypeptide (PP), glucagon, and insulin from the isolated canine pancrease. Somatostatin in picomolar doses potently inhibited insulin and glucagon secretion, whereas PP secretion was relatively insensitive. Also, in the absence of acetylcholine, somatostatin exerted a preferential inhibition of the release insulin and glucagon compared with PP. These findings point to a physiologically important role of somatostatin for the secretion of insulin and glucagon, but probably not for PP.

Acetylcholine↗
PubMed1979

The influence of calcium on the basal and acetylcholine-stimulated secretion of pancreatic polypeptide.

The influence of calcium on basal and acetylcholine-stimulated pancreatic polypeptide (PP) secretion was investigated in an isolated pancreatico-duodenal preparation and compared to the secretion of glucagon and insulin. The stimulatory effect of 5 mmol/liter calcium on PP release was of the same magnitude as that obtained by 5 mmol/liter arginine or 10 nmol/liter isoproterenol but only one fifth of the PP response to acetycholine (1 mumol/liter). All stimuli were equipotent with respect to insulin and glucagon release. The acetylcholine (1 mumol/liter)-stimulated PP release was almost identical at calcium concentrations of 1.3 and 6.3 mmol/liter, whereas glucagon release was calcium dependent, with higher responses at high (6.3 mmol/liter) than at normal (1.3 mmol/liter) calcium concentrations. In a calcium-depleted medium, acetylcholine induced a prompt, short-lived, but repeatable PP response, whereas no increase in glucagon or insulin was found. Further, when calcium influx into cells was blocked by excess magnesium (5.0 mmol/liter), the basal and acetylcholine (1 mumol/liter)-stimulated PP secretion was only inhibited by 12% (P = NS) and 42% (2P less than 0.05), respectively, whereas glucagon release was inhibited 56% (2P less than 0.001) and 76% (2P less than 0.01), respectively. It is concluded that the secretion of PP is influenced by calcium ions; however, the PP release is much less dependent on extracellular calcium ions than are insulin and glucagon secretions.

Acetylcholine↗
PubMed1979

Characterization of somatostatin release from the pancreas: the role of potassium.

The effect of potassium on somatostatin secretion from the isolated perfused canine pancreas was studied. Potassium stimulated dose-dependent somatostatin release in a monophasic response pattern. The effect of potassium was abolished in the absence of calcium. Perfusion of 1 micronmol/l atropine and 1 micronmol/l propranolol was without effect on the potassium induced somatostatin release. The results suggest that the stimulatory effect of potassium on somatostatin release is secondary to increases in calcium influx into the D cell. The sympathetic and parasympathetic nerve endings in the pancreas are apparently not involved in the potassium mediated secretory processes.

Adrenergic beta-Antagonists↗
PubMed1978

Pancreatic polypeptide, glucagon and insulin secretion from the isolated perfused canine pancreas.

The release of pancreatic polypeptide (PP) by gut hormones, acetyl choline and adrenaline was investigated in an isolated perfused pancreas preparation. PP was potently released by 1 nmol/1 caerulein (186 +/- 12%, p is less than 0.001) and gastric inhibitory peptide (GIP) (211 +/- 31%, p is less than 0.005) as well as by 1 mumol/1 acetyl choline (1097 +/- 59%, p is less than 0.001). A significant two-fold release of PP was also evoked by 1 nmol/1 vasoactive intestinal peptide (VIP) (129 +/- 38%, p is less than 0.02 and gastrin (108 +/- 25% p is less than 0.01). Insulin release, induced by high glucose concentration was enhanced by both GIP (210 +/- 38%, p is less than (0.01) and VIP (48 +/- 5%, p is less than 0.001). In addition GIP enhanced the release of glucagon by 179 +/- 18% (p is less 0.001) at 1.4 mmol/1 glucose and by 127 +/- 24% (p is less than 0.005) at 8.3 mmol/1 glucose. Thus no simple inter-relationship appears to exist between the control of the three circulating islet hormones.

Acetylcholine↗
PubMed1978

Dual action of mn++ upon the secretion of insulin and glucagon from the isolated, perfused canine pancreas. Possible interactions with ca++.

Since Mn++ apparently interferes with excitation-contraction coupling by both reducing inward movement of Ca++ across the cell membrane and by displacing Ca++ from an intracellular store, studies were performed in the isolated, perfused canine pancreas to elucidate the existence of a similar effect in stimulus-secretion coupling and to draw comparisons with the effect of Mg++, which antagonizes Ca++ at the cell membrane. The results show: 1. than Mn++ (0.05, 0.125, and 0.25 mmol/l) inhibits the release of insulin and glucagon in a dose dependent fashion during the first 3-4 min of infusion followed by a dose-dependent increase in hormone release, the 'escape phase'. 2. The inhibitory action of Mn++ (0.25 mmol/l) upon release of both hormones is progressively counteracted when perfusate calcium is increased from 0.7 to 1.3 to 5.0 mmol/l. 3. Mg++ (5 mmol/l) inhibits the release of both hormones with no sign of an 'escape phase'. 4. Mn++ (0.5 mmol/l) during calcium depletion causes a gradual stimulation of the release of both hormones. The dual action of Mn++ upon hormone release from the endocrine pancreas suggests that Mn++ can cross the cell membrane and can interfere with stimulus-secretion coupling both at the membrane level, by competitively inhibiting the Ca++ influx, and at some intracellular level by releasing calcium from an intracellular store.

Animals↗
PubMed1978

Haloperidol, a dopaminergic antagonist: somatostatin-like inhibition of glucagon and insulin release from the isolated, perfused canine pancreas.

The effect of haloperidol, a dopaminergic antagonist, on insulin and glucagon secretion was investigated using the isolated, perfused canine pancreas. Haloperidol at 4 X 10(-7) to 10(-5) mol/l caused a dose-dependent inhibition of glucagon release both at low (25 mg/100 ml) and high glucose concentrations (150 mg/100 ml). At the low glucose concentration insulin release was already maximally suppressed. At the high glucose concentration haloperidol (4 X 10(-7) to 10(-5) mol/1) also caused a dose-dependent inhibition of insulin release. Haloperidol (10(-5) mol/1) inhibited dramatically pancreatic A and B cell responses to isoproterenol (2 ng/ml), acetylcholine (1 mumol/1) and arginine (5 mmol/1). The inhibitory effect of haloperidol on both glucagon and insulin release could be eliminated by increasing perfusate calcium concentration from 1.3 to 8.8 mmol/1. These findings suggested that haloperidol blocks glucagon and insulin release in a somatostatin-like manner by affecting a fundamental step of the stimulus-secretion coupling, probably by interfering with calcium handling of the pancreatic A and B cells.

Acetylcholine↗
PubMed1977

Pharmacodynamics of a new selective beta2-adrenergic bronchodilator 3-(4-methoxybenzylamino)-4-hydroxy-alpha-(tert. butylaminomethyl)-benzyl-alcohol, HCl (QH25).

The bronchodilator effect of QH25 (3-(4-methoxybenzylamino)-4-hydroxy-alpha-(tert. butylaminomethyl)benzylalcohol, HCl) a new beta2-adrenergic bronchodilator has been investigated in conscious guinea pigs and in anaesthetized guinea pigs and cats and compared to that of salbutamol and isoprenaline. In anaesthetized guinea pigs QH25 and isoprenaline were equipotent after intravenous administration, whereas salbutamol was four times less active. The same difference between QH25 and salbutamol was observed after intraduodenal administration. After oral administration in conscious guinea pigs QH25 was eight and five times more potent than salbutamol and isoprenaline respectively, whereas no difference was observed when the agents were administered as aerosols. The bronchodilator action of QH25 was apprxomately three times that of salbutamol in egg-albumine sensitized guinea pigs after oral administration. In anaesthetized cats the bronchodilator potency of QH25 was three times that of salbutamol and the same or slightly higher than that of isoprenaline. A half-life of 4 hours for the bronchodilator action in guinea pigs was determined for both QH25 and salbutamol after oral administration. The effect of QH25 and salbutamol on cardiovascular parameters i.e. chrono- and inotropic action and blood pressure decreasing effect in guinea pigs, cats and dogs was essentially the same whereas isoprenaline was from 5 to 30 times more potent. The potential tremorogenic action of QH25 estimated on the cat soleus muscle was eight times less than that of isoprenaline and the same or slightly less than that of salbutamol. From the experimental data it is concluded that QH25 has the same potency as isoprenaline as a bronchodilator agent but is more potent than salbutamol. Taking into account that isoprenaline is considerably more active on cardiovascular parameters and on the cat soleus muscle than QH25 which has the same or less effect than salbutamol on these parameters the data suggest that QH25 is a more selective bronchodilator agent than both isoprenaline and salbutamol.

Acetylcholine↗
PubMed1977

Effect of Verapamil on pancreatic glucagon release from the isolated, perfused canine pancreas.

The effect of Verapamil, a potent calcium antagonist, upon pancreatic glucagon release was investigated in the isolated, perfused canine pancreas. Verapamil at concentrations ranging between 10(-5)-10(-4) mol/l caused a dose-related inhibition of glucagon release at a glucose concentration of 25 mg/dl. The inhibition was an immediate and reversible phenomenon. The inhibitory effect was reduced when the Ca2+ concentration was increased from 1.3 to 5.0 mmol/l. The results are compatible with earlier findings from our laboratory demonstrating that calcium plays a key role in the stimulus-secretion coupling of glucagon release.

Animals↗
PubMed1975

Beta-adrenergic mechanisms and ulcer formation in pylorus-ligated rats.

The importance of beta-adrenergic receptor activity for ulcer formation was studied. In rats fasted for 48 hours, ulcers in the rumen were produced constantly after 17 hours of pyloric ligation. d,1,Propranolol in doses of 1 to 30 mg/kg given 4 times during 12 hours caused a dose-dependent inhibition of ulcer formation. The ulcero-protective potency of d,1,propranolol was about 20 times that of d,propranolol. No explanation of the ulcero-protective effect was observed when the gastric acid secretion was studied after 17 hours. Serum gastrin concentration after 17 hours of ligation was in all animals less than 5 pmol per liter, i.e. below one-third of the normal fasting value. For all pharmacological effects apart from beta-adrenergic blockage, d,1, and d,propranolol do not differ, while the results presented here suggest that intact beta-adrenergic receptor activity is important for the development of gastric ulcers in the pylorus-ligated rat. The mechanism behind the ulcero-protective effect of beta-adrenergic blockage remains to be solved.

Animals↗