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Review
. 2006;2(2):163-9.
doi: 10.2147/vhrm.2006.2.2.163.

Leptin and hypertension in obesity

Paco E Bravo  1 , Stephen Morse, David M Borne, Erwin A Aguilar, Efrain Reisin
Affiliations
Review

Leptin and hypertension in obesity

Paco E Bravo et al. Vasc Health Risk Manag. 2006.

Abstract

Leptin, a peptide discovered more than 10 years ago, decreases food intake and increases sympathetic nerve activity to both thermogenic and non-thermogenic 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 non-thermogenic 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.

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Figures

Figure 1
Figure 1
Renal and blood pressure effect of leptin. Adapted from Hall et al 2001. Copyright © 2001. Reproduced with permission from Hall JE, Hildebrandt DA, Kuo J. 2001. Obesity hypertension: role of leptin and sympathetic nervous system. Am J Hypertension, 14(6 Pt 2):103S-115S.
Figure 2
Figure 2
Potential pathways in which obesity can cause cardiovascular dysfunction. Effects of obesity-hypertension on the heart. Adapted from Zhang et al 2000. Copyright © 2004. Reproduced with permission from Zhang R, Reisin E. 2000. Obesity-hypertension: the effects on cardiovascular and renal systems. Am J Hypertens, 13:1308-14. Abbreviations: BP, blood pressure; CHF, congestive heart failure; CO, cardiac output; LV, left ventricular; NP, natriuretic peptides; RAS, renin–angiotensin system; SNS, sympathetic nervous system.
See this image and copyright information in PMC

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