• 1 January 1979
    • journal article
    • research article
    • Vol. 26  (5) , 399-406
Abstract
The .beta.2 adrenergic agonist salbutamol was infused i.v. in doses of 0.05, 0.1 and 0.2 .mu.g/kg per min in conscious dogs with gastric fistulae. Salbutamol inhibited meal-stimulated acid (measured with intragastric tiltration) by up to 82%. Salbutamol produced dose-related inhibition of acid stimulated by pentagastrin (up to 88R) and by histamine (up to 52%). Pepsin secretion in response to histamine (but no pentagastrin) was inhibited by salbutamol. The salbutamol infusion caused a marked tachycardia, an increase in pulse pressure, slight hyperkalemia and hyperglycemia. The .beta.-adrenergic antagonist propranolol augmented pentagastrin-stimulated acid and inhibited meal-stimulated secretion. Propranolol abolished salbutamol induced tachycardia, and blocked the inhibition by salbutamol of pentagastrin-stimulated acid. Salbutamol inhibittion of acid in the dog supports the hypothesis that there are .beta.2-adrenergic receptors in the stomach.