Histamine H2-receptor antagonists cimetidine and oxmetidine, H2-receptor agonist dimaprit, H1-receptor antagonist chlorpheniramine and H1-receptor agonist 2-thiazolylethylamine were tested for their effects on unstimulated pancreatic exocrine secretion in anaesthetized rabbits fitted with an acute pancreatic cannula. Intravenous administration of H1 agonist induces a dose-dependent increase in pancreatic secretion but H1 antagonist have the opposite effects. Intravenous administration of H2 antagonists induces effects similar the ones produced after H1 agonist infusion. The implications of H1 and H2 receptors on exocrine pancreatic secretion are discussed.
SUMMARYAn investigation was made of the effects of HI and H2 receptor agonists and antagonists on rabbit pancreatic exocrine secretion stimulated by secretin and cholecystokinin (CCK). The HI agonist 2-thiazolylethylamine elicited dose-dependent increases in the rate of secretion. Increases in pancreatic juice flow and enzyme output were also noted after H2 antagonist cimetidine. In contrast, the HI antagonist chlorpheniramine and H2 agonist dimaprit caused reductions in flow and enzyme output. The results suggest that HI receptors have stimulative effects and H2 receptors have inhibitory effects on exocrine rabbit pancreas.
Effects of pirenzepine, known as a muscarinic receptor antagonist, on the contraction of dog gallbladder elicited by cholecystokinin (CCK) were examined in comparison with atropine and hexamethonium ones. Intraluminal gallbladder pressure in an in situ anaesthetized dog model was chosen for studying gallbladder motility. The intravenous administration of pirenzepine (0.75 mg/kg b.wt.), atropine (3 mg/kg b.wt.) or hexamethonium (5 mg/kg b.wt.) elicited a marked decrease in the increase of intraluminal gallbladder pressure induced by intravenous bolus injections of CCK (0.25-2 Ivy dog unit/kg b.wt.) and by continuous infusion of CCK (0.025-0.4 Ivy dog unit/kg b.wt./min). It was concluded that CCK induced gallbladder contractions were influenced by both nicotinic and muscarinic receptors.
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