Chronic Cardiovascular and Renal Actions of Leptin: Role of Adrenergic Activity
Abstract
Abstract— This study was designed to determine the role of changes in adrenergic activity in mediating the chronic cardiovascular, renal, and metabolic actions of leptin. Male Sprague-Dawley rats were implanted with catheters for mean arterial pressure (MAP) and heart rate (HR) measurements and IV infusions of either vehicle (n= 7) or α- and β-adrenergic receptor antagonists, terazosin and propranolol (10 mg/kg/d; n= 8) throughout the study. After control measurements, murine leptin was infused IV (1.0 μg/kg/min) for 7 days along with vehicle or adrenergic antagonists, followed by a 7-day recovery period. Leptin infusion significantly reduced food intake in control rats from 22.6±0.8 to 10.6±0.4 g/d and, in adrenergic blockade rats, from 22.6±0.8 to 13.2±0.8 g/d. Fasting plasma insulin decreased from 48±10 to 5±2 μU/mL in control rats and from 51±9 to 9±2 μU/mL in adrenergic blockade rats during leptin infusion. Leptin infusion did not significantly alter glomerular filtration rate in either group. MAP and HR increased by 6±1 mm Hg and 23±7 bpm after 7 days of leptin infusion in control rats. However, in adrenergic blockade rats, leptin infusion did not significantly alter MAP (−1±1 mm Hg) and decreased, rather than increased, HR (−23±8 bpm). These results indicate that leptin-induced increases in blood pressure and tachycardia are mediated by increased adrenergic activity and support the concept that leptin may be an important link between obesity, increased sympathetic activity, and hypertension. However, the chronic effects of leptin on insulin and glucose regulation do not appear to be altered by α- and β-adrenergic receptor blockade.
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Combined blockade of both α-adrenergic and β-adrenergic receptors abolished the chronic effects of leptin on blood pressure in male rats, suggesting that these effects were mediated by the sympathetic nervous system.
“Combined blockade of both a-adrenergic and β-adrenergic receptors abolished the chronic effects of leptin on BP in male rats, suggesting that these effects were mediated by the SNS128.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [128]
Administration of α/β-adrenergic blockers or clonidine prevents most of the obesity-induced rise in BP in obese animals, and α/β-adrenergic blockade reduces ambulatory BP significantly more in obese than in lean hypertensive patients.
“administration of α/β-adrenergic blockers or clonidine, which stimulates central α-2 adrenergic receptors and reduces SNS activity, prevents most of the obesity-induced rise in BP in obese animals10,62 and α/β-adrenergic blockade reduces ambulatory BP significantly more in obese than in lean hypertensive patients63”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [62]
The BP effects of leptin were completely abolished by combined α/β-adrenergic receptor blockade.
“The BP effects of leptin were completely abolished by combined α/β-adrenergic receptor blockade”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [62]
Leptin requires activation of POMC neurons and MC4R to mediate its effects on renal sympathetic nervous system activity and blood pressure.
“Leptin requires activation of POMC neurons and MC4R to mediate its effects on renal SNS activity and BP [28, 50, 51].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [51]
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- Authors
- Carlyle, M., Jones, O. B., Kuo, J. J., & Hall, J. E.
- Affiliations
- University of Mississippi Medical Center (US)
- Venue
- Hypertension
- Published
- 2002-02
- Volume
- 39
- Issue
- 2
- Pages
- 496-501
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2072436009
- Cited by
- 292
- References
- 22
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 2 · 2023: 6 · 2022: 13 · 2021: 11 · 2020: 8 · 2019: 13 · 2018: 4 · 2017: 21 · 2016: 21 · 2015: 13 · 2014: 18 · 2013: 10 · 2012: 16
- FWCI
- 4.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- National Heart, Lung, and Blood Institute (P01-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 › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- leptin, adrenergic activity, alpha-blockers, beta-blockers, terazosin, propranolol, blood pressure, heart rate, dietary intake, insulin, glucose regulation, glomerular filtration rate, obesity, sympathetic nervous system
- MeSH terms
- Adrenergic Agonists, Animals, Blood Pressure, Disease Models, Animal, Drug Interactions, Eating, Heart Rate, Hormones, Kidney, Kidney Function Tests, Male, Pressoreceptors, Receptors, Adrenergic, Tachycardia, Rats, Sprague-Dawley, Adrenergic Antagonists, Leptin, Rats
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