P-539: Preservation of the arterial pressure response to leptin in diet-induced obese mice: A potential mechanism for obesity hypertension

Kamal Rahmouni; Gina M Morgan; Donald A Morgan; Allyn L Mark; William G Haynes

doi:10.1016/j.amjhyper.2005.03.556

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P-539: Preservation of the arterial pressure response to leptin in diet-induced obese mice: A potential mechanism for obesity hypertension

Journal article

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P-539: Preservation of the arterial pressure response to leptin in diet-induced obese mice: A potential mechanism for obesity hypertension

Kamal Rahmouni, Gina M Morgan, Donald A Morgan, Allyn L Mark and William G Haynes

American journal of hypertension, Vol.18(S4), pp.203A-203A

05/2005

DOI: 10.1016/j.amjhyper.2005.03.556

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Abstract

We have previously demonstrated that diet-induced obese mice have selective resistance to leptin with preservation of the renal sympathetic nerve activity response to leptin despite loss of the feeding- and weight-reducing actions of leptin. The preserved renal sympathetic response to leptin associated with the hyperleptinemia observed in mice on high fat diet might be expected to increase arterial pressure in these obese mice. To test the ability of leptin to increase arterial pressure in the obese mice we compared the action of intraperitoneal administration of leptin in mice on normal chow and high fat diet for 10 weeks. Radiotelemetric mean arterial pressure (MAP) was recorded in the conscious unrestrained state for 7 days. Lean and obese mice then received 12 days treatment with vehicle or leptin (60 mg, twice daily, IP) with continued MAP recordings. After 10 weeks, mice on high fat diet weighed about 10% more than those fed the normal chow (30.8±0.2 vs.27.9±0.2 g, P<0.001). Mice on high fat diet showed higher baseline MAP than the mice on normal chow (110±1 vs. 100±1 mmHg, P<0.001). In mice on normal chow, 12-day leptin treatment caused a significant increase in MAP as expected (+9±6 and -2±2.mmHg for leptin- and vehicle-treated mice respectively, P<0.001). Leptin caused also a significant increase in MAP in the high fat-fed mice (+6±5 vs. -5±1 mmHg, P<0.01). Leptin treatment caused a significant decrease in body weight, food intake and fat mass in mice on normal chow, but not in the high fat-fed mice. This study demonstrates that there is preservation of the arterial pressure response to leptin in a dietary model of obesity despite resistance to the appetite and weight reducing actions of leptin. This represents a potential mechanism for increases in arterial pressure and adverse cardiovascular actions of leptin in obesity.

Hypertension

Obesity

Leptin

Details

Title: Subtitle: P-539: Preservation of the arterial pressure response to leptin in diet-induced obese mice: A potential mechanism for obesity hypertension
Creators: Kamal Rahmouni - Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA
Gina M Morgan - Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA
Donald A Morgan - Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA
Allyn L Mark - Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA
William G Haynes - Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA
Resource Type: Journal article
Publication Details: American journal of hypertension, Vol.18(S4), pp.203A-203A
DOI: 10.1016/j.amjhyper.2005.03.556
ISSN: 0895-7061
eISSN: 1879-1905
Publisher: Oxford University Press
Language: English
Date published: 05/2005
Academic Unit: Iowa Neuroscience Institute; Neuroscience and Pharmacology; Internal Medicine
Record Identifier: 9984072078702771

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