Functional roles of adrenoceptors in parietal cells were pharmacologically investigated using isolated canine parietal cells. In the crude membranes obtained from preparations highly purified in parietal cells ( > 95% of purity), the specific binding of [3H]dihydroalprenolol (DHA) was observed with a Kd value of 2.9 nM and Bmax of 234 fmol/mg protein, while the specific binding of [3H]prazosin and [3H]rauwolscine were not attained. Propranolol concentration-dependently reduced the specific binding of [3H]dihydroalprenolol with a Ki value of 2.6 nM. Isoproterenol concentration-dependently stimulated [14C]aminopyrine accumulation in preparations enriched in parietal cells (about 70% purity) with the maximum at 10 nM. Isoproterenol increased the content of cyclic AMP in preparations enriched in parietal cells (70%) with the maximum at 100 nM. The isoproterenol-induced stimulatory effect of [14C]aminopyrine accumulation in preparations enriched in parietal cells (70%) was completely abolished by 1 μM propranolol but not by 1 μM phentolamine. In the presence of 1 μM propranolol, 100 μM noradrenaline did not affect carbachol- and histamine-induced [14C]aminopyrine accumulation in preparations enriched in parietal cells (70%). The present study suggests that stimulation of β-adrenoceptors located on canine parietal cells evokes acid production in a cyclic-AMP-dependent manner. Furthermore, a possibility arises that canine parietal cells are not the site of action of α-adrenoceptors in mediating inhibition of gastric acid secretion.
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