The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Chronic Leptin Infusion Increases Arterial Pressure
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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In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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”
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Sowers, J. R., & Frohlich, E. D. (2004) · Medical Clinics of North America · doi:10.1016/s0025-7125(03)00128-7 · Cited by 1,528
Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms
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Insulin Resistance and Chronic Cardiovascular Inflammatory Syndrome
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Metadata
- Authors
- Shek, E. W., Brands, M. W., & Hall, J. E.
- Affiliations
- University of Mississippi Medical Center (US)
- Venue
- Hypertension
- Published
- 1998-01
- Volume
- 31
- Issue
- 1
- Pages
- 409-414
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- 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 › Endocrinology, Diabetes and Metabolism › 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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