Back to Journals » Vascular Health and Risk Management » Volume 2 » Issue 2

Leptin and hypertension in obesity

Authors Paco E Bravo, Stephen Morse, David M Borne, Erwin A Aguilar, Efrain Reisin

Published 15 June 2006 Volume 2006:2(2) Pages 163—169

Download Article [PDF] 

Paco E Bravo1, Stephen Morse1, David M Borne2, Erwin A Aguilar1, Efrain Reisin1

1Sections of Nephrology and 2Comprehensive Medicine, Department of Internal Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA

Abstract: Leptin, a peptide discovered more than 10 years ago, decreases food intake and increases sympathetic nerve activity to both thermogenic and nonthermogenic tissue. Leptin was initially believed to be an anti-obesity hormone, owing to its metabolic effects. However, obese individuals, for unknown reasons, become resistant to the satiety and weight-reducing effect of the hormone, but preserve leptin-mediated sympathetic activation to nonthermogenic tissue such as kidney, heart, and adrenal glands. Leptin has been shown to influence nitric oxide production and natriuresis, and along with chronic sympathetic activation, especially to the kidney, it may lead to sodium retention, systemic vasoconstriction, and blood pressure elevation. Consequently, leptin is currently considered to play an important role in the development of hypertension in obesity.

Keywords: leptin, renal sympathetic nerve activity, blood pressure, obesity, selective leptin resistance, nitric oxide, natriuresis

Download Article [PDF]