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Cited by 686Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesBlood Pressure and Hypertension Studies

Chronic Leptin Infusion Increases Arterial Pressure

Shek, Eugene W., Brands, Michael W., Hall, John E.·1998·Hypertension
DOI 10.1161/01.hyp.31.1.409
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Abstract

Plasma leptin concentration is increased in hypertensive obese humans, but whether leptin contributes to the increased arterial pressure in obesity is not known. In this study, we tested whether chronic increases in leptin, to levels comparable to those in obesity, could cause a sustained increase in arterial pressure and also the importance of central nervous system (CNS) versus systemic mechanisms. Five male Sprague-Dawley rats were implanted with chronic nonoccluding catheters in the abdominal aorta and both carotid arteries for CNS infusion, and five other rats were implanted with an abdominal aorta catheter and femoral vein catheter for intravenous (IV) infusion. After 7 days of control, leptin was infused into the carotid arteries or femoral vein at 0.1 μg/kg/min for 5 days and 1.0 μg/kg/min for 7 days, followed by a 7-day recovery period. The carotid artery and IV infusions of leptin at 1μg/kg/min significantly increased plasma leptin levels, from 1.2 ± 0.4 ng/mL to 91 ± 5 ng/mL and from 0.9 ± 0.1 ng/mL to 94 ± 9 ng/mL, respectively, but there was no significant increase in either group at the low dose. Food intake also did not change at the low dose but decreased by approximately 65% in the carotid group and 69% in the IV group after 7 days of the 1 μg/kg/min infusion. Mean arterial pressure (MAP) increased slightly at the low dose only in the carotid group, but this was not statistically significant. At the higher dose, however, MAP increased significantly from 86 ± 1 mm Hg to 94 ± 1 mm Hg in the carotid group and from 87 ± 1 mm Hg to 93 ± 1 mm Hg in the IV group. Heart rate also increased significantly in both groups at 1 μ/g/kg/min leptin infusion. Fasting blood glucose and insulin levels decreased significantly at 1 μg/kg/min in both the carotid artery group (−10.5% and −82.5%, respectively) and the IV group (−13.6% and −80.4%, respectively). All variables returned to control levels after leptin infusion was stopped. These results indicate that chronic increases in circulating leptin cause sustained increases in arterial pressure and heart rate and are consistent with a possible role for leptin in obesity hypertension.

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Crossref · 10.1161/01.hyp.31.1.409

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  • Leptin infusions in rodents over several days cause mild, gradual increases in blood pressure and heart rate.

    “Leptin infusions in rodents over several days also cause mild, gradual increases in BP and HR125–127.”

    From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [125]

  • Chronic increases in plasma leptin levels comparable to severe obesity caused sustained increases in BP and HR in rodents.

    “We demonstrated, however, that chronic increases in plasma leptin levels, comparable to those found in severe obesity, caused sustained increases in BP and HR in rodents87.”

    From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [87]

  • Chronic increases in plasma leptin levels, comparable to those found in severe obesity, caused sustained increases in blood pressure and heart rate in rodents despite causing weight loss.

    “Acute leptin administration in rodents and humans increases renal and muscle SNS activity [45, 46] while chronic increases in plasma leptin levels, comparable to those found in severe obesity, caused sustained increases in BP and HR in rodents despite causing weight loss which would normally reduce BP [47].”

    From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [47]

  • When infused into animals, leptin raises blood pressure, stimulates the sympathetic nervous system, and correlates with blood pressure in at least some human populations.

    “When infused into animals, leptin raises the BP, 27 stimulates the SNS, 28 and has been shown to correlate with BP, in at least some human populations.29,30”

    From Obesity‐Related Hypertension: Pathogenesis, Cardiovascular Risk, and Treatment: A Position Paper of <i>The Obesity Society</i> and the <i>American Society of Hypertension</i> (2013) · cites this paper as [27]

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Authors
Shek, E. W., Brands, M. W., & Hall, J. E.
Affiliations
University of Mississippi Medical Center (US)
ORCID
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1998-01
Volume
31
Issue
1
Pages
409-414
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/01.hyp.31.1.409
OpenAlex
W2126412697
Cited by
686
References
17
Citations by year
2026: 5 · 2025: 2 · 2024: 7 · 2023: 7 · 2022: 7 · 2021: 12 · 2020: 12 · 2019: 13 · 2018: 13 · 2017: 23 · 2016: 23 · 2015: 22 · 2014: 19 · 2013: 26 · 2012: 32
FWCI
13.55
Type
journal article
Language
en
Open access
closed
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (HL‐51971, P01HL051971)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
Keywords
leptin, arterial pressure, obesity, intravenous infusion, heart rate, insulin, blood glucose, dietary intake, plasma leptin, rats, neuroendocrine regulation of blood pressure, sympathetic nervous system, renin-angiotensin system, renin-angiotensin-aldosterone system
MeSH terms
Aldosterone, Animals, Aorta, Abdominal, Blood Glucose, Blood Pressure, Brain, Carotid Arteries, Corticosterone, Feeding Behavior, Femoral Vein, Glomerular Filtration Rate, Heart Rate, Infusions, Intra-Arterial, Infusions, Intravenous, Insulin, Kidney, Male, Obesity, Proteins, Regional Blood Flow, Renin, Sodium, Time Factors, Vascular Resistance, Rats, Sprague-Dawley, Leptin, Rats

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