ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Bombesin-like receptor 3 regulates blood pressure and heart rate via a central sympathetic mechanism.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Divergent activation patterns of BRS3 revealed by two Chinese herb-derived agonists.Acta pharmaceutica Sinica. B · 2025Article
- scRNA-seq data from the larval Drosophila ventral cord provides a resource for studying motor systems function and development.Developmental cell · 2024Article
- GAmerican journal of physiology. Endocrinology and metabolism · 2021Article
- Pilot study and bioinformatics analysis of differentially expressed genes in adipose tissues of rats with excess dietary intake.Molecular medicine reports · 2020Article
- The Catalytic SubunitJournal of the Endocrine Society · 2019Article
- Brs3 neurons in the mouse dorsomedial hypothalamus regulate body temperature, energy expenditure, and heart rate, but not food intake.Nature neuroscience · 2018Article
- Receptor-specific crosstalk between prostanoid E receptor 3 and bombesin receptor subtype 3.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Bombesin receptor subtype-3-expressing neurons regulate energy homeostasis through a novel neuronal pathway in the hypothalamus.Brain and behavior · 2018Article
- Bombesin-like receptor 3 (Brs3) expression in glutamatergic, but not GABAergic, neurons is required for regulation of energy metabolism.Molecular metabolism · 2017Article
- Bombesin-Like Receptor 3: Physiology of a Functional Orphan.Trends in endocrinology and metabolism: TEM · 2016Review
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bombesin-like receptor 3 (BRS-3) is an orphan G protein-coupled receptor that regulates energy expenditure, food intake, and body weight. We examined the effects of BRS-3 deletion and activation on blood pressure and heart rate. In free-living, telemetered Brs3 null mice the resting heart rate was 10% lower than wild-type controls, while the resting mean arterial pressure was unchanged. During physical activity, the heart rate and blood pressure increased more in Brs3 null mice, reaching a similar heart rate and higher mean arterial pressure than control mice. When sympathetic input was blocked with propranolol, the heart rate of Brs3 null mice was unchanged, while the heart rate in control mice was reduced to the level of the null mice. The intrinsic heart rate, measured after both sympathetic and parasympathetic blockade, was similar in Brs3 null and control mice. Intravenous infusion of the BRS-3 agonist MK-5046 increased mean arterial pressure and heart rate in wild-type but not in Brs3 null mice, and this increase was blocked by pretreatment with clonidine, a sympatholytic, centrally acting α2-adrenergic agonist. In anesthetized mice, hypothalamic infusion of MK-5046 also increased both mean arterial pressure and heart rate. Taken together, these data demonstrate that BRS-3 contributes to resting cardiac sympathetic tone, but is not required for activity-induced increases in heart rate and blood pressure. The data suggest that BRS-3 activation increases heart rate and blood pressure via a central sympathetic mechanism.
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