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This Article Full Text Full Text (PDF) All Versions of this Article: 91/3/603    most recent expphysiol.2005.032755v1 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 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. Related Collections Vascular

¹ Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia, Università del Piemonte Orientale ‘A. Avogadro’, via Solaroli 17, I-28100 Novara, Italy

Regional intra-arterial infusion of human placental lactogen in anaesthetized pigs has been shown to cause coronary, renal and iliac vasoconstriction by antagonizing the vasodilatory effects of ß₂-adrenergic receptors. Since nitric oxide is known to modulate or mediate ß₂-adrenergic effects, the present study was planned in the same experimental model to determine the role of nitric oxide in the above vascular responses to human placental lactogen. In eight pigs anaesthetized with sodium pentobarbitone, changes in anterior descending coronary, left renal and left internal iliac blood flow caused by intra-arterial infusion of human placental lactogen at constant heart rate and arterial blood pressure were assessed using electromagnetic flowmeters. Intra-arterial infusion of the human placental lactogen caused decreases in coronary, renal and iliac blood flow which, respectively, averaged 16.7, 8.1 and 12.2% of the baseline values. The role of nitric oxide in this response was studied in the same pigs by repeating the experiments, after measured blood flows had returned to baseline values, following intra-arterial administration of N-nitro-L-arginine methyl ester (L-NAME). The subsequent intra-arterial infusion of human placental lactogen did not cause any significant changes in measured blood flows, even when performed after reversing the increase in arterial blood pressure and coronary, renal and iliac resistance caused by L-NAME with continuous intravenous infusion of papaverine. These results indicate that the coronary, renal and iliac vasoconstriction caused by human placental lactogen, known to involve antagonism of ß₂-adrenergic vasodilatory effects, was mediated by inhibition of nitric oxide release.

(Received 11 November 2005; accepted after revision 27 February 2006; first published online 2 March 2006)
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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