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Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173, Japan
We examined the role
and the peripheral mechanism of action of central dopamine on basal
pancreatic exocrine secretion in conscious rats. Rats were fitted with
bile and pancreatic catheters to collect bile and pancreatic juice
separately and also with a left lateral brain ventricle and external
jugular vein catheters. After 90-min basal collection, the
D1- and
D2-receptor antagonists (Sch-23390
and eticlopride, respectively) and dopamine were administered into the
lateral brain ventricle. Sch-23390 (30, 100, and 300 nmol/rat), but not eticlopride (300 nmol/rat), stimulated pancreatic fluid and protein secretion. Dopamine (30, 100, and 300 nmol/rat) inhibited pancreatic secretion dose dependently. Pretreatment with
Sch-23390 prevented the inhibitory effect of dopamine. Intravenously injected Sch-23390 or dopamine had no effect on pancreatic secretion. The inhibitory effect of dopamine was blocked by bretylium, an inhibitor of norepinephrine release, and phentolamine, an
-blocker, but not by vagotomy. The
-antagonist propranolol alone
significantly inhibited basal pancreatic secretion, and dopamine did
not modify the inhibitory effect of propranolol. The proton pump
inhibitor omeprazole partially but not completely reduced the
inhibition by dopamine. These results suggest that central dopamine
inhibits pancreatic exocrine secretion via
D1-like receptors and that the inhibitory effect is mediated via sympathetic nerves, especially
-adrenoceptors.
intracerebroventricular administration; pancreatic exocrine
secretion; D1-like receptor; sympathetic nerve;
-adrenoceptor
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