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This Article Full Text Full Text (PDF) All Versions of this Article: 89/4/363    most recent expphysiol.2004.027334v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Grossini, E. Articles by Vacca, G. Search for Related Content PubMed PubMed Citation Articles by Grossini, E. Articles by Vacca, G. Related Collections Cardiovascular control

Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia, Università del Piemonte Orientale ‘A. Avogadro’, via Solaroli 17, I-28100 Novara, Italy

Infusion of insulin in anaesthetized pigs has been shown to cause an increase in renal blood flow and a decrease in coronary blood flow, which were the net result of a vasoconstriction involving sympathetic -adrenoceptor-mediated mechanisms and of a local vasodilatation involving the endothelial release of nitric oxide. In the present study, the effect of insulin on superior mesenteric blood flow was examined in pentobarbitone-anaesthetized pigs at constant heart rate, aortic blood pressure, left ventricular contractility and blood levels of glucose and potassium. In 10 pigs, infusion of 0.004 IU kg ^–1 min^–1 of insulin increased mesenteric flow. In five of these pigs, intravenous phentolamine enhanced the increase in mesenteric flow elicited by insulin, a response which was abolished by the subsequent injection of N-nitro-L-arginine methyl ester (L-NAME) into the mesenteric artery. In the remaining five pigs, infusion of insulin after intramesenteric injection of L-NAME caused a decrease in mesenteric flow. This response was abolished by the subsequent intravenous administration of phentolamine. The present study showed that infusion of insulin in anaesthetized pigs primarily caused a mesenteric vasodilatation, which was the net result of two opposite effects, namely a predominant vasodilatation mediated by the endothelial release of nitric oxide and a sympathetic vasoconstrictor mechanism mediated by -adrenoceptors.

(Received 2 February 2004; accepted after revision 18 March 2004; first published online 1 April 2004)
Corresponding author E. Grossini, Facoltà di Medicina e Chirurgia, via Solaroli 17, I-28100 Novara, Italy. Email: grossini{at}med.unipmn.it