ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Endogenous leptin contributes to baroreflex suppression within the solitary tract nucleus of aged rats.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Leptin excites basolateral amygdala principal neurons and reduces food intake by LepRb-JAK2-PI3K-dependent depression of GIRK channels.Journal of cellular physiology · 2024Article
- The retrotrapezoid nucleus and the neuromodulation of breathing.Journal of neurophysiology · 2021Review
- Interplay Between Systemic Metabolic Cues and Autonomic Output: Connecting Cardiometabolic Function and Parasympathetic Circuits.Frontiers in physiology · 2021Review
- Heart Rate Variability and Cardiovascular Fitness: What We Know so Far.Vascular health and risk management · 2021Review
- Hatano rats are a suitable metabolic syndrome model for studying feeding behavior, blood pressure levels, and percent body fat.The Journal of veterinary medical science · 2019Article
- Facilitation of breathing by leptin effects in the central nervous system.The Journal of physiology · 2016Review
- Comorbidity Factors and Brain Mechanisms Linking Chronic Stress and Systemic Illness.Neural plasticity · 2016Review
- Alterations in the Medullary Endocannabinoid System Contribute to Age-related Impairment of Baroreflex Sensitivity.Journal of cardiovascular pharmacology · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The decline in cardiovagal baroreflex function that occurs with aging is accompanied by an increase in circulating leptin levels. Our previous studies showed that exogenous leptin impairs the baroreflex sensitivity for control of heart rate in younger rats, but the contribution of this hormone to baroreflex dysfunction during aging is unknown. Thus we assessed the effect of bilateral leptin microinjection (500 fmol/60 nl) within the solitary tract nucleus (NTS) on the baroreflex sensitivity in older (66 ± 2 wk of age) urethane/chloralose anesthetized Sprague-Dawley rats with elevated circulating leptin levels. In contrast to the 63% reduction observed in younger rats, leptin did not alter the baroreflex sensitivity for bradycardia evoked by phenylephrine in older rats (0.76 ± 0.19 baseline vs. 0.71 ± 0.15 ms/mmHg after leptin; P = 0.806). We hypothesized that this loss of sensitivity reflected endogenous suppression of the baroreflex by elevated leptin, rather than cardiovascular resistance to the peptide. Indeed, NTS administration of a leptin receptor antagonist (75 pmol/120 nl) improved the baroreflex sensitivity for bradycardia in older rats (0.73 ± 0.13 baseline vs. 1.19 ± 0.26 at 10 min vs. 1.87 ± 0.32 at 60 min vs. 1.22 ± 0.54 ms/mmHg at 120 min; P = 0.002), with no effect in younger rats. There was no effect of the leptin antagonist on the baroreflex sensitivity for tachycardia, responses to cardiac vagal chemosensitive fiber activation, or resting hemodynamics in older rats. These findings suggest that the actions of endogenous leptin within the NTS, either produced locally or derived from the circulation, contribute to baroreflex suppression during aging.
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