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This Article Full Text Full Text (PDF) All Versions of this Article: 90/5/689    most recent expphysiol.2005.030775v1 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 Montanaro, M. S Articles by Oldfield, B. J Search for Related Content PubMed PubMed Citation Articles by Montanaro, M. S Articles by Oldfield, B. J Related Collections Cardiovascular control Symposia Papers

¹ Howard Florey Institute² Department of Physiology, University of Melbourne, Victoria 3010, Australia ³ Department of Physiology, Monash University, Victoria 3800, Australia

Abstract

Leptin, a peptide hormone normally associated with body weight homeostasis, is implicated in the generation of obesity-induced hypertension. Administration of leptin increases sympathetic nerve activity and blood pressure; however, the neural circuity involved in this pressor effect is not clearly defined. In this review we describe experiments in which pseudorabies virus was injected into the heart, kidney and the vasculature within skeletal muscle to reveal the distribution of neurones in the hypothalamus that project to these cardiovascular tissues. This distribution is compared to the well-documented distribution of leptin receptors. Finally we discuss microinjection studies designed to examine the effect of leptin, in these regions, on sympathetic nerve discharge and arterial blood pressure. Leptin injected directly into the ventromedial hypothalamus, arcuate nucleus and lateral hypothalamic area (particularly the perifornical area) increased lumbar sympathetic nerve activity. In addition, microinjection into the ventromedial hypothalamus and parvocellular paraventricular nucleus increased blood pressure. Our results demonstrate a discrete set of hypothalamic pathways that may underlie the involvement of leptin in obesity-induced hypertension.

(Received 6 July 2005; accepted after revision 29 July 2005; first published online 16 August 2005)
Corresponding author A. Allen: Department of Physiology, University of Melbourne, Victoria 3010, Australia. Email: a.allen{at}unimelb.edu.au

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