EFFECTS OF β‐ADRENOCEPTOR DRUG STIMULATION ON VARIOUS MODELS OF GASTRIC ULCER IN RATS

Abstract

1 Experiments were designed to evaluate the effect of the pharmacological activation of β-adrenoceptors on various models of gastric ulcer in the rat. 2 Pretreatment with the β-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 β₂-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 β-adrenoceptor agonists exert preventive and curative effects on gastric damage induced in the rat. This effect seems specific and mediated through β-adrenoceptor activation.