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Response to Role of Hyperleptinemia in the Regulation of
Blood Pressure and Cardiac Function
King’s College London
King’s Health Partners
London, United Kingdom
Downloaded from http://hyper.ahajournals.org/ by guest on June 17, 2017
We appreciate Dr Tsuda’s comments and observations on the
involvement of nitric oxide in leptin-induced endothelial dysfunction
and cardiac failure. We agree with Dr Tsuda that similar mechanisms
might occur in neonatal leptin–treated rats. Because endothelial dysfunction represents an early form of vascular disease that precedes
other cardiovascular complications, the role of neonatal leptin on
endothelial function may provide valuable mechanistic insights.
Although we will be proposing to conduct these analyses, we will
also investigate the role of the overactive sympathetic nervous system in the neonatal leptin–treated rats,1 which may influence vascular
tone and cardiac function. Recent study by Wang et al2 demonstrates
that endothelial dysfunction in leptin-induced mice is blocked by
mesenteric sympathetic denervation. Interestingly, also superoxide
scavanger TEMPOL (4-hydroxy-2,2,6,6-tetrametylpiperidin-1-oxyl)
treatment had similar therapeutic effects and suggests reactive oxygen
species and sympathetic outflow as potential targets for leptin-induced
endothelial dysfunction and hypertension.2
Leptin has also shown a negative inotropic effect in the heart,
which has been shown to be dependent on nitric oxide and STAT-3
(signal transducer and activator of transcription 3)–induced p38
mitogen–activated protein kinase activation.3,4 These mechanistic
pathways will be considered in future work, as well as potential targets, which mediate the adverse cardiac effects secondary to neonatal
hyperleptinemia.
James Clark
Olena Rudyk
Michael J. Shattock
Cardiovascular Division
King’s College London
King’s Health Partners
London, United Kingdom
Sung Eun Bae
Timothy South
Joaquim Pombo
Kathrine Redington
Esna Uppal
Clive W. Coen
Lucilla Poston
Paul D. Taylor
Division of Women’s Health
Women's Health Academic Centre
King’s College London
King’s Health Partners
London, United Kingdom
Sources of Funding
1. Samuelsson AM, Clark J, Rudyk O, Shattock MJ, Bae SE, South T, Pombo J,
Redington K, Uppal E, Coen CW, Poston L, Taylor PD. Experimental hyperleptinemia in neonatal rats leads to selective leptin responsiveness, hypertension, and altered myocardial function. Hypertension. 2013;62:627–633.
2. Wang J, Wang H, Luo W, Guo C, Wang J, Chen YE, Chang L, Eitzman
DT. Leptin-induced endothelial dysfunction is mediated by sympathetic
nervous system activity. J Am Heart Assoc. 2013;2:e000299.
3. Wold LE, Relling DP, Duan J, Norby FL, Ren J. Abrogated leptin-induced
cardiac contractile response in ventricular myocytes under spontaneous
hypertension: role of Jak/STAT pathway. Hypertension. 2002;39:69–74.
4. Nickola MW, Wold LE, Colligan PB, Wang GJ, Samson WK, Ren J.
Leptin attenuates cardiac contraction in rat ventricular myocytes. Role of
NO. Hypertension. 2000;36:501–505.
This study was supported by the British Heart Foundation
(FS/10/003/28163) and Biotechnology and Biological Sciences
Research Council (BBD5231861).
Disclosures
None.
Anne-Maj Samuelsson
Division of Women’s Health
Women’s Health Academic Centre
(Hypertension. 2014;63:00-00.)
© 2013 American Heart Association, Inc.
Hypertension is available at http://hyper.ahajournals.org
DOI: 10.1161/HYPERTENSIONAHA.113.02399
e1
Response to Role of Hyperleptinemia in the Regulation of Blood Pressure and Cardiac
Function
Anne-Maj Samuelsson, James Clark, Olena Rudyk, Michael J. Shattock, Sung Eun Bae,
Timothy South, Joaquim Pombo, Kathrine Redington, Esna Uppal, Clive W. Coen, Lucilla
Poston and Paul D. Taylor
Downloaded from http://hyper.ahajournals.org/ by guest on June 17, 2017
Hypertension. published online November 25, 2013;
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2013 American Heart Association, Inc. All rights reserved.
Print ISSN: 0194-911X. Online ISSN: 1524-4563
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http://hyper.ahajournals.org/content/early/2013/11/25/HYPERTENSIONAHA.113.02399.citation
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