BIBER, B., J. FARA and 0. LUNDGREN. A pharmacological study of intestinal vasodilator mechanisms in the cat. Acta physiol. scand. 1974. 90. 673-683. The intestinal vasodilator responses evoked by close i.a. administration of cholecystokinin ( C C K ) and secretin, mechanical stimulation of the mucosa and transmural electrical field stimulation were abolished by the 5-hydroxytryptamine (5-HT) antagonist dihydroergotamine, given in doses sufficient to block the vascular effects of i.a. injected 5-HT. Corresponding results were obtained by making the cat small intestine tachyphylactic to 5-HT. Nervous blockade (tetrodotoxin) , inhibiting the intestinal blood flow increase after mechanical mucosal or electrical field stimulation, left the vascular responses to exogenous CCK and secretin unaffected. An increased 5-HT content in venous blood from the intestine was demonstrated during vasodilatations caused by electrical field stimulation. A participation of intestinal 5-HT, possibly as a transmitter substance, in the vasodilator mechanism evoked by mechanical mucosal stimulation o r electrical transmural field stimulation is suggested.Mesenteric blood flow increases following instillation of fat or acid into the duodenum, due at least in part to the release and action of the duodenal hormones cholecystokinin (CCK) and secretin (Fara, Rubinstein and Sonnenschein 1972).Further, mechanical stimulation of the intestinal mucosa causes an intestinal vasodilator response suggested to be mediated through a local intestinal nervous reflex (Biber, Lundgren and Svanvik 1971). Also, nervous structures in the intestinal wall can be directly activated by transmural electrical field stimulation (Biber, Fara and Lundgren 1973 a ) , causing an intestinal vasodilatation. Thus it seems likely that different trigger mechanisms are involved in rhe local regulation of intestinal blood flow.The question of whether a common mediator mechanism might be involved in the above mentioned intestinal vascular responses has been raised by several recent studies involving 5-hydroxytryptamine (5-HT ) and tetrodotoxin. The normal intestinal wall contains abundant amounts of 5-HT (Vialli 1966), and local i.a. administration of 5-HT evokes an intestinal vasodilator response, which regarding its effects on the consecutive vascular sections, closely resembles that induced by 3-743003. Acta physiol. scand. Vol. 90: 4 673
Gastric inhibitory polypeptide (GIP) inhibits histamine-, pentagastrin-, and insulinstimulated gastric acid secretion (I) and potentiates glucose-stimulated insulin release (2). This recently described gastrointestinal peptide has 43 amino acids and 15 of the first 26 occur in the same position as porcine glucagon while 9 of these 26 are in the same position as in porcine secretin (3). While both glucagon (4) and secretin (5, 6) have been shown to produce mesenteric vasodilation, vascular actions of GIP have not been reported. However, GIP is released from the small intestine in response to intraluminal glucose (7) and fat (8), stimuli which have been previously associated with an increase in mesenteric blood flow (6, 9). Thus, this study was done to investigate the effects of GIP on superior mesenteric and femoral blood flow and also intestinal motility in the anesthetized cat. Our results indicate that GIP increases superior mesenteric blood flow, and possible physiological implications are discussed.Materials and methods. Cats weighing between 2.0 and 3.6 kg were fasted for 18 hr and then anesthetized with pentobarbital 40 mg/kg. The left femoral artery and vein were cannulated to record arterial pressure and to inject drugs, respectively, after which a laparotomy was performed. Blood flow in the superior mesenteric and right femoral arteries was recorded with noncannulating Biotronex electromagnetic flow meter probes and flow meter. Zero-flow levels were obtained using miniature occluders ( 10). Mesenteric arterial vascular resistance was calculated by dividing mean systemic arterial pressure by mean su-'
Introduction of milk or corn oil into the duodenum of the cat evokes an increase in superior mesenteric blood flow (blocked by atropine), an inhibition of gastric and duodenal motility, and sedation. Cholecystokinin-pancreozymin mimics the mesenteric vascular effect of intraduodenal fat and seems to have a sedating action.
This study demonstrates that for the isolated cat gall bladder a smaller molar dose of the sulfated form of OP-CCK and gastrin is required to produce contraction as compared to the respective non-sulfated forms. For OP the D50 for the sulfated form versus the non-sulfated form was 1.94. For gastrin it was 1.10.
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