K. Bech

Effect of dopamine on pentagastrin-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula by using miniature strain-gauge transducers. Infusion of pentagastrin changed the contractile activity to a digestive state. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade or adrenergic and dopaminergic receptors. The stimulated antral motility was inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone and by cis-flupenthixol, which blocks both peripheral and central dopaminergic receptors. The effect of dopamine was not significantly altered by the beta 1-adrenoceptor blocker practolol, the alpha-adrenoceptor blocker phentolamine, or the alpha + beta-adrenoceptor blocker labetalol. Consequently, this study indicates that dopamine acts on gastric antral motility through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, seem not to be involved in the motility response.

Effect of Somatostatin on Bethanechol-Stimulated Gastric Acid Secretion and Gastric Antral Motility in Dogs with Gastric Fistula

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha-adrenergic, beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.

Effect of Dopamine on Pentagastrin-Stimulated Gastric Acid Secretion and Mucosal Blood Flow in Dogs with Gastric Fistula

The purpose of this study was to elucidate the effect of intravenously administered dopamine on dopamine receptors and adrenergic receptors in terms of its effect on gastric acid secretion, the kinetic mechanism, blood flow, and antral motility. Dopamine was used alone and in conjunction with selective blockade of alpha-, beta-, and dopaminergic receptors. A significant inhibition of gastric acid secretion was found with the highest dose of dopamine used (40 micrograms/kg/min). The kinetic study showed characteristics of a non-competitive type. The anti-secretory effect dopamine was significantly blocked by non-selective beta-blockade or by selective beta-blockade but not by alpha- or dopaminergic receptor blockade. This suggests that the inhibitory effect of dopamine on gastric secretion is mediated by beta-receptors. There was no significant effect on gastric mucosal blood flow, but the ratio between blood flow and acid secretion was significantly elevated during dopamine infusion, indicating that the acid inhibition was not secondary to changes in blood flow. It is concluded that the dopamine inhibition of acid secretion is mediated by beta 1-receptors, unlike the effect on antral gastric motility, which is mediated by dopamine receptors.

Effect of Isoprenaline on Pentagastrin-Stimulated Gastric Acid Secretion in Dogs with Gastric Fistula

The purpose of this study was to elucidate the effect of a beta 1-adrenoceptor agonist on gastric acid secretion in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist was used alone and in conjunction with selective blockade of beta 2- and beta 1-receptors. Isoprenaline dose-dependently inhibited the secretory volume and the acidity. The antisecretory effect of isoprenaline was significantly blocked by the beta 1-adrenoceptor blocker practolol and by the beta 1 + beta 2-adrenoceptor blocker propranolol but not by H 35/25, a beta 2-adrenoceptor blocker. This indicates that isoprenaline acts on the acid secretion exclusively through beta 1-receptors. Dose-response experiments with five logarithmically increased doses of pentagastrin and one dose of isoprenaline showed unchanged calculated maximum response and an increase in half-maximum acid response. It is concluded that the inhibitory effect of isoprenaline on gastric acid secretion is of competitive or uncompetitive type.

Effect of serotonin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs.

The purpose of the present study was to evaluate the effect of serotonin on bethanechol-stimulated gastric acid secretion and antral motility in conscious dogs with gastric fistula. Bethanechol stimulated the acid secretion dose-dependently and maintained the frequency and strength of the antral contractions at a high level. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was stimulated. The acid inhibition was blocked by propranolol, and dose-response analysis showed inhibition of a non-competitive type. This study thereby shows that serotonin inhibits bethanechol-stimulated gastric acid secretion similarly to salmefamol (beta 2-adrenergic agonist)--that is, dose-dependently and non-competitively. Serotonin has been proposed to be a mediator of the beta-adrenergic influence on gastric function in vivo, but the counteracting effect of propranolol and the stimulatory effect of serotonin on motility contradict this hypothesis.

Effect of Dopamine on Bethanechol-Stimulated Gastric Antral Motility in Dogs with Gastric Fistula

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility with regard to both frequency and strength. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone. The alpha-adrenoceptor blocker phentolamine reduced the effect of dopamine to some extent, but the reduction was not of statistical significance. The dopamine-inhibited motility was not altered by the beta 1-adrenoceptor blocker practolol or the beta 1 + beta 2-adrenoceptor blocker propranolol. This indicates that dopamine acts on gastric antral motility predominantly through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, do not seem to be involved in the motility response. Dose-response investigations with five increasing doses of bethanechol and one dose of dopamine showed inhibition of a non-competitive type.

Effect of Somatostatin on Histamine-Stimulated Gastric Acid and Pepsin Secretion in Dogs

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and pepsin secretion in conscious dogs with gastric fistula. Infusion of histamine stimulated dose-dependently the acid secretion, whereas pepsin secretion was decreased by the high doses of histamine. Somatostatin inhibited dose-dependently the stimulated acid secretion but only with a maximum of 40%. The pepsin secretion was inhibited by somatostatin dose-dependently and with a higher potency. The acid inhibition was of a competitive type and prostaglandin-independent.

Somatostatin Increases the Ratio between Gastric Mucosal Blood Flow and Gastric Acid and Pepsin Secretion in Dogs

The effects of somatostatin on gastric mucosal blood flow (GMBF), acid secretion, and pepsin secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method for estimating the mucosal blood flow. Somatostatin inhibited the pentagastrin- and bethanechol-stimulated gastric acid and pepsin secretion and resulted in an absolute decrease in mucosal blood flow. The ratios between GMBF and secretion (acid and pepsin) were increased during somatostatin infusion, which suggests a relative increase in mucosal blood flow and independent inhibition of gastric secretion. It may be concluded from this study that the acid- and pepsin-inhibitory effects of somatostatin are not mediated by changes in the GMBF.

Exogenous Serotonin and Histamine-Stimulated Gastric Acid and Pepsin Secretion in Dogs

The effects of serotonin on histamine-stimulated gastric acid and pepsin secretion were evaluated in conscious dogs with a gastric fistula. Histamine stimulated the acid secretion dose-dependently, whereas pepsin secretion was decreased by the high doses of histamine. The acid secretion was inhibited slightly by serotonin, with a maximum of 42% with a dose of 10 micrograms/kg/min. The pepsin secretion was only decreased non-significantly by serotonin, 10-15 micrograms/kg/min. The acid inhibition was counteracted by beta-adrenergic antagonists (propranolol, atenolol) and methysergide (serotonergic antagonist). The dose-response analysis showed inhibition of a competitive type. In conclusion, serotonin inhibits histamine-stimulated gastric acid secretion via serotonergic receptors and beta-adrenoceptors, whereas pepsin secretion is unaffected.

Effect of Serotonin on Bethanechol-Stimulated Gastric Pepsin Secretion in Dogs

The effect of serotonin on bethanechol-stimulated gastric pepsin secretion was evaluated with regard to dose-response kinetics and receptor mediation. A low dose of exogenous serotonin produced a stimulation (0.5 microgram/kg/min), whereas inhibition was found for higher doses (5-10 micrograms/kg/min). The inhibition was non-competitive and could be significantly counteracted by beta-adrenergic blocking drugs. This study confirms results obtained during pentagastrin stimulation and supports the concept that serotonin acts via sympathetic nerves to release noradrenaline.