Effect of Sympathomimetic Amines on the Histamine Forming Capacity of Human Leucocytes

I The effect of isoprenaline on gastric secretion evoked by various means has been studied in conscious rats provided with Pavlov and Heidenhain pouches. 2 Interdigestive acid secretion in the Pavlov pouch was reduced by isoprenaline, whereas pepsin secretion was unaltered.3 Central vagal stimulation effected by 2-deoxy-D-glucose injection evoked a gastric secretory response that was substantially reduced by isoprenaline. 4 2-Deoxy-D-glucose increased the mobilization of gastric mucosal histamine, an effect that was prevented by isoprenaline. 5 Isoprenaline infusion alone induced a slight increase in histamine mobilization and also a considerable elevation of immunoreactive serum gastrin concentration. 6 The secretory response to food in the Pavlov pouch was almost abolished by isoprenaline. 7 Although the acid response to histamine in the Heidenhain pouch was susceptible to isoprenaline inhibition, that to methacholine was not. 8 Pepsin secretion in the Heidenhain pouch preparation stimulated by histamine or methacholine seemed to be enhanced by isoprenaline.

Section: Discussionsupporting

confidence: 53%

Further Studies on the Mode of Action of Isoprenaline on Gastric Secretion in the Conscious Rat

Lundell

Svensson

Nilsson

1976

“…The antiulcer effect elicited by salbutamol in the pylorus-ligation model may also be related to a restrictive activity on histamine formation (Assem & Feigenbaum, 1972;Lundell & Svensson, 1974). In fact, this mechanism has been previously suggested by Curwain et al (1974) to explain the antisecretory effects of ,B-adrenoceptor agonists.…”

Section: Discussionmentioning

confidence: 96%

Effects of Β‐adrenoceptor Drug Stimulation on Various Models of Gastric Ulcer in Rats

Esplugues

Lloris

Martí-Bonmatí

et al. 1982

1 Experiments were designed to evaluate the effect of the pharmacological activation of fadrenoceptors on various models of gastric ulcer in the rat.2 Pretreatment with the P-adrenoceptor stimulant drugs, isoprenaline or salbutamol, significantly inhibited stress-induced gastric ulcers. This anti-ulcer effect was abolished by propranolol but not by atenolol, suggesting that P2-adrenoceptors mediate this response.3 In the pylorus-ligation model, salbutamol inhibited lesion formation and reduced the intragastric content of hydrogen ions, histamine and pepsin although the latter was only affected with the higher dose of salbutamol.4 Salbutamol also prevented the ulcerogenic action on the gastric mucosa of an exogenously perfused artificial gastric juice, showing that the anti-ulcer effect is not necessarily dependent on acid inhibition. 5 Salbutamol also reduced the formation of acute ulcers induced by various iatrogenic means (histamine, polymyxin B, reserpine and indomethacin). 6 Long-term treatment with salbutamol accelerated the healing of experimental chronic gastric ulcer.7 In anaesthetized rats, salbutamol produced a dose-related increase in mucosal blood flow which may contribute to its mode of action.8 It is concluded that P-adrenoceptor agonists exert preventive and curative effects on gastric damage induced in the rat. This effect seems specific and mediated through P-adrenoceptor activation.

“…Agonists of (-receptors have been reported to inhibit histamine release from sensitized lung tissue (Assem & Schild, 1969, 1971 and reduce the rate of histamine formation in sensitized human leucocytes (Assem & Feigenbaum, 1972).…”

Section: Discussionmentioning

confidence: 99%

“…Evidence is accumulating to show that the mobilization of preformed mucosal histamine and accelerated synthesis of the amine are functionally linked to the excitation of the parietal cell (for references, see Kahlson, Rosengren & Svensson, 1973). Isoprenaline has been found to inhibit the release of histamine from sensitized lung tissue (Assem & Schild, 1969, 1971) and inhibit histamine formation in sensitized human leucocytes (Assem & Feigenbaum, 1972). This ,-receptor agonist readily inhibits pentagastrininduced acid secretion in the dog, whereas that produced by histamine is relatively insensitive to isoprenaline (Curwain & Holton, 1972).…”

Section: Introduction Methodsmentioning

confidence: 99%

Implication of Gastric Mucosal Histamine in Inhibition by Isoprenaline of Pentagastrin‐induced Gastric Secretion

Lundell

Svensson

1974

The effect of isoprenaline on pentagastrin‐induced gastric secretion was studied in conscious rats with Heidenhain pouches. The influence of isoprenaline on pentagastrin‐induced release and formation of gastric mucosal histamine was also examined. Isoprenaline strongly inhibited pentagastrin‐induced acid secretion, an inhibition which could not be overcome by increasing the dose of pentagastrin. Propranolol blocked the inhibitory effect of isoprenaline on pentagastrin‐induced acid secretion. Isoprenaline enhanced pepsin secretion induced by pentagastrin, an effect which was blocked by propranolol. Isoprenaline reduced the increase in formation and release of gastric mucosal histamine following pentagastrin infusion, an inhibitory influence which was almost completely blocked by propranolol. The inhibition by isoprenaline of pentagastrin‐induced acid secretion is tentatively related to alterations in gastric mucosal histamine occurring simultaneously.