Inhibition of NO Synthesis Enhances Chronic Cardiovascular and Renal Actions of Leptin
Abstract
Acute studies suggest that leptin has pressor and depressor actions, including stimulation of sympathetic activity as well as increased release of NO from the vascular endothelium. The goal of this study was to examine the role of NO in modulating the chronic blood pressure, heart rate, and renal responses to hyperleptinemia, comparable to that found in obesity-induced hypertension. Male Sprague-Dawley rats were implanted with arterial and venous catheters, and mean arterial pressure and heart rate were monitored continuously 24 h/d. After a 4-day control period, the rats were infused with isotonic saline vehicle (n=6) or N G -nitro- l -arginine methyl ester (L-NAME, 10 μg/kg per minute; n=9) to inhibit NO synthesis for 7 days. After 7 days of vehicle or L-NAME administration, leptin was infused intravenously for 7 days at a rate of 0.5 μg/kg per minute, followed by a leptin infusion at 1.0 μg/kg per minute for 7 days, along with vehicle or L-NAME. A 21-day infusion of L-NAME alone (n=6) served as a control for the L-NAME+leptin rats. Although the low dose of leptin alone did not significantly elevate arterial pressure, it raised the heart rate by 18±3 bpm. The higher leptin infusion rate raised arterial pressure from 96±3 to 104±3 mm Hg but did not increase the heart rate further. L-NAME+leptin increased arterial pressure by 40±6 mm Hg and heart rate by 79±19 bpm compared with pretreatment levels. In control L-NAME rats, mean arterial pressure increased by 31±4 mm Hg, whereas the heart rate was not altered significantly compared with pretreatment levels. Neither chronic leptin infusion alone nor L-NAME alone altered the glomerular filtration rate or renal plasma flow significantly, but L-NAME+leptin reduced glomerular filtration rate by 27±11% and renal plasma flow by 47±9%. These results indicate that impaired NO synthesis mildly enhances the chronic renal hemodynamic and hypertensive effects of leptin but markedly amplifies the tachycardia caused by hyperleptinemia.
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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 [127]
The chronic hypertensive effects of leptin in non-obese rodents are modest; however, hyperleptinaemia also causes anorexia and stimulates nitric oxide production, effects that tend to decrease sympathetic nerve activity and blood pressure.
“The chronic hypertensive effects of leptin in non-obese rodents are modest; however, hyperleptinaemia also causes anorexia and stimulates NO production, effects that tend to decrease SNA and BP127.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [127]
The chronic hypertensive effects of leptin were greatly potentiated after inhibition of nitric oxide synthesis despite weight loss that was associated with decreased food intake.
“The chronic hypertensive effects of leptin were greatly potentiated after inhibition of NO synthesis despite weight loss that was associated with decreased food intake127.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [127]
Leptin stimulates NO production, which opposes increases in BP.
“Moreover, leptin stimulates NO production which opposes increases in BP.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [86]
Acute injections of leptin have little effect on BP despite increasing SNS activity.
“acute injections of leptin have little effect on BP despite increasing SNS activity”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [86]
After blocking NO synthesis, the chronic effects of leptin to cause hypertension and tachycardia were markedly amplified despite reduced food intake and weight loss.
“After blocking NO synthesis the chronic effects of leptin to cause hypertension and tachycardia were markedly amplified despite reduced food intake and weight loss86.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [86]
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- Authors
- Kuo, J. J., Jones, O. B., & Hall, J. E.
- Affiliations
- University of Mississippi Medical Center (US)
- Venue
- Hypertension
- Published
- 2001-02
- Volume
- 37
- Issue
- 2
- Pages
- 670-676
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2096229046
- Cited by
- 114
- References
- 25
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 4 · 2019: 3 · 2018: 1 · 2017: 3 · 2016: 6 · 2015: 7 · 2014: 3 · 2013: 6 · 2012: 3
- FWCI
- 6.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- National Heart, Lung, and Blood Institute (PO1HL-51971, 51971, HL‐51971, P01HL051971)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- leptin, nitric oxide synthesis inhibition, L-NAME, hyperleptinemia, obesity-related hypertension, blood pressure, heart rate, tachycardia, glomerular filtration rate, renal plasma flow, renal hemodynamics, endothelium-dependent relaxation
- MeSH terms
- Animals, Blood Pressure, Cardiovascular System, Drinking, Eating, Glomerular Filtration Rate, Heart Rate, Infusions, Intravenous, Kidney, Male, Nitric Oxide, Potassium, Sodium, Tachycardia, Rats, Sprague-Dawley, Renal Plasma Flow, Nitric Oxide Synthase, NG-Nitroarginine Methyl Ester, Leptin, Rats
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