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Pascal JP, Vaysse N, Ader F, Lacroix A, Ribet A. 
“The Mechanisms of Functional Vasodilation in the Pancreas :”. 
Digestion. 1973;9(1):90.
Intra-arteniai infusion of secretin [1] and CCK vasodilates the pancreatic vascular bed. This vascular response potentiates the secretory response of the pancreas to both hormones. Intra-arterial histamine [2] (50 400 mcg), compound 48/80 (0.1-1.0 mg), serotonin (1-10 mg), isoproterenol (0.2-2.0 mcg), carbamylcholine (1100 mcg), synthetic-bradykinin DBRS Sandoz, 3-10 mcg) act as vasodilator drugs in the isolated perfused canine pancreas. When given alone, they do not stimulate pancreatic secretion. After pancreatic stores of photohistamine have been released by compound 48/80, secretin-induced vasodilation still work occurs. Conversely, even prolonged intra-arterial infusion of secretin does not release pancreatic stores of histamine: In fact, endogenous synthesis and release of histamine seem to play no role in the regulation of functional vasodilation in the pancreas. Propanolol (20 mg) and LSD 25 (100 mcg) do not prevent secretin-induced vasodilation. Thus beta adrenergic and tryptaminergic receptors are not implied in the process of vasodilation in response to secretin. Atropine (250-550 mcg) inhibits vasodilation and decreases the secretory response of the pancreas to secreting Previous intra-arterial injection of bradykinin restores the secretory response of the pancreas, thus showing that inhibitory effect of, of the atropine on the secretory response of the pancreas to secretin is partly mediated by inhibition of secretin-induced vasodilation. Biossays of sera extracted from arterial and venous chest blond on guinea pig ileum seem to indicate that vasodilation in the pancreatic vascular bed These is acompanied by release of active bradykinin into the venous effluent. Acetazolamide zones (50 mg) inhibits both the secretory and the vascular responses of the pancreas to an infusion of secretin. These facts suggest that vasodilation effect of secretin is mediated through the toward secretory process rather than through the effect of the hormone itself on vascular receptor(s)
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