Autonomic nervous control of pancreatic somatostatin secretion.
We studied the autonomic nervous control of pancreatic somatostatin secretion using isolated perfused pig pancreases prepared with either intact vagal or splanchnic nerve supply. Electrical stimulation of the vagus nerves increased pancreatic protein output 59-fold, whereas somatostatin output decreased to 57% of prestimulatory secretion. Acetylcholine mimicked the somatostatin response to vagal stimulation, and atropine abolished the inhibition. Splanchnic nerve stimulation increased perfusion pressure up to threefold, whereas somatostatin output decreased to 68%. Phenoxybenzamine abolished the pressure response to splanchnic nerve stimulation and reversed the inhibition to a 20% increase in somatostatin output. Propranolol did not influence the inhibitory effect of splanchnic stimulation but abolished the increase seen after phenoxybenzamine. It is concluded that both divisions of the autonomic nerve supply to the pancreas are inhibitory to somatostatin secretion, but increased secretion may be brought about by a beta-adrenergic mechanism.
D000818:Animals; D004558:Electric Stimulation; D007700:Kinetics; D010179:Pancreas / Q000187:drug effects / Q000294:innervation*; D010189:Pancreatic Juice / Q000187:drug effects / Q000378:metabolism*; D010477:Perfusion; D010643:Phenoxybenzamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D013004:Somatostatin / Q000378:metabolism*; D013153:Splanchnic Nerves / Q000502:physiology*; D013552:Swine; D014630:Vagus Nerve / Q000502:physiology*
D010643:Phenoxybenzamine; D013004:Somatostatin; D011433:Propranolol