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This Article Full Text Full Text (PDF) All Versions of this Article: 557/1/307    most recent jphysiol.2004.063354v1 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Molinari, C. Articles by Vacca, G. Search for Related Content PubMed PubMed Citation Articles by Molinari, C. Articles by Vacca, G.

Laboratorio di Fisiologia, Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia, Università del Piemonte Orientale ‘A. Avogadro’, Novara, Italy

Dehydroepiandrosterone has been implicated in vascular disease and its associated insulin resistance and hypertension, though little is known about its vascular effects. We have recently shown in prepubertal anaesthetized pigs that intravenous infusion of dehydroepiandrosterone caused coronary vasoconstriction through the inhibition of a vasodilatory ß-adrenergic receptor-mediated effect related to the release of nitric oxide. The present study was designed to investigate the effect of dehydroepiandrosterone on mesenteric, renal and iliac vascular beds. In prepubertal pigs of both sexes anaesthetized with sodium pentobarbitone, changes in superior mesenteric, left renal and left external iliac blood flow caused by intravenous infusion of dehydroepiandrosterone were assessed using electromagnetic flowmeters. Changes in heart rate and arterial blood pressure were prevented by atrial pacing and by connecting the arterial system to a pressurized reservoir containing Ringer solution. In 22 pigs, infusion of 1 mg h^–1 of dehydroepiandrosterone decreased mesenteric, renal and iliac blood flow. In a further 10 pigs, dose–response curves were obtained by graded increases in the infused dose of hormone between 0.03 and 4 mg h^–1. The mechanisms of the above response were studied in the 22 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. Blockade of -adrenoceptors with intravenous phentolamine (five pigs) did not affect the dehydroepiandrosterone-induced mesenteric, renal and iliac vasoconstriction. This response was abolished by blockade of ß₂-adrenoceptors with intravenous butoxamine (five pigs) and by blockade of mesenteric, renal and iliac nitric oxide synthase with intra-arterial administration of N-nitro-L-arginine methyl ester (seven pigs), even after reversing the increase in local vascular resistance caused by the two blocking agents with intravenous infusion of papaverine. In five pigs, the increase in measured blood flow caused by intravenous infusion of isoproterenol (isoprenaline) was significantly reduced by infusion of dehydroepiandrosterone. The present study showed that intravenous infusion of dehydroepiandrosterone primarily caused mesenteric, renal and iliac vasoconstriction. The mechanisms of this response were shown to be due to the inhibition of a vasodilatory ß₂-adrenergic receptor-mediated effect, which possibly involved the release of nitric oxide.

(Received 25 February 2004; accepted after revision 16 March 2004; first published online 19 March 2004)
Corresponding author C. Molinari: Facoltà di Medicina e Chirurgia, Via Solaroli 17, I-28100 Novara, Italy. Email: molinari{at}med.unipmn.it

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