ArticleKidney international2016
β3 adrenergic receptor in the kidney may be a new player in sympathetic regulation of renal function.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- New perspectives on thick ascending limb function and cell types.Kidney international · 2026Review
- Transient acute kidney injury following femoral fracture in mice : the role of sympathetic activation.Bone & joint research · 2026Article
- β3-AR/β-arrestin2 Interaction Triggers Cardiac Fibrosis Through JNK/c-Jun Pathway in Cardiac Fibroblasts.Journal of cellular and molecular medicine · 2026Article
- Transcriptional regulatory factors of the Aqp2 gene.Kidney research and clinical practice · 2026Article
- Protective Effects of Selective β-Adrenoceptor Blockade on Renal Pathophysiology in a Catecholamine Storm of Rat.International journal of molecular sciences · 2026Article
- HIF1A, ADRB3, and VEGFA gene expression in human cord blood across gestation: insights toward a pharmacological artificial placenta.Pediatric research · 2026Article
- Causal Association Between Commonly Used Medicines and Diabetes-Related Eye Diseases: Univariable and Multivariable Mendelian Randomization Study.Journal of diabetes research · 2026Article
- βBiochemistry research international · 2025Review
- The β3-AR agonist BRL37344 ameliorates the main symptoms of X-linked nephrogenic diabetes insipidus in the mouse model of the disease.Journal of cellular and molecular medicine · 2024Article
- The βAdvances in pharmacological and pharmaceutical sciences · 2024Review
- β3-Adrenoceptor as a new player in the sympathetic regulation of the renal acid-base homeostasis.Frontiers in physiology · 2024Article
- Is the βBiomolecules · 2023Review
- TRPML1-Induced Lysosomal CaInternational journal of molecular sciences · 2023Article
- β3 Adrenergic Receptor Agonist Mirabegron Increases AQP2 and NKCC2 Urinary Excretion in OAB Patients: A Pleiotropic Effect of Interest for Patients with X-Linked Nephrogenic Diabetes Insipidus.International journal of molecular sciences · 2023Article
- Morphology of Schwann Cell Processes Supports Renal Sympathetic Nerve Terminals With Local Distribution of Adrenoceptors.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Subcellular distribution of α2-adrenoceptor subtypes in the rodent kidney.Cell and tissue research · 2022Article
- Suppression of estrogen receptor beta classical genomic activity enhances systemic and adipose-specific response to chronic beta-3 adrenergic receptor (β3AR) stimulation.Frontiers in physiology · 2022Article
- Emerging therapies for autosomal dominant polycystic kidney disease with a focus on cAMP signaling.Frontiers in molecular biosciences · 2022Review
- β3 adrenergic receptor as potential therapeutic target in ADPKD.Physiological reports · 2021Article
- Activation of the Thiazide-Sensitive Sodium-Chloride Cotransporter by Beta3-Adrenoreceptor in the Distal Convoluted Tubule.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
To date, the study of the sympathetic regulation of renal function has been restricted to the important contribution of β1- and β2-adrenergic receptors (ARs). Here we investigate the expression and the possible physiologic role of β3-adrenergic receptor (β3-AR) in mouse kidney. The β3-AR is expressed in most of the nephron segments that also express the type 2 vasopressin receptor (AVPR2), including the thick ascending limb and the cortical and outer medullary collecting duct. Ex vivo experiments in mouse kidney tubules showed that β3-AR stimulation with the selective agonist BRL37344 increased intracellular cAMP levels and promoted 2 key processes in the urine concentrating mechanism. These are accumulation of the water channel aquaporin 2 at the apical plasma membrane in the collecting duct and activation of the Na-K-2Cl symporter in the thick ascending limb. Both effects were prevented by the β3-AR antagonist L748,337 or by the protein kinase A inhibitor H89. Interestingly, genetic inactivation of β3-AR in mice was associated with significantly increased urine excretion of water, sodium, potassium, and chloride. Stimulation of β3-AR significantly reduced urine excretion of water and the same electrolytes. Moreover, BRL37344 promoted a potent antidiuretic effect in AVPR2-null mice. Thus, our findings are of potential physiologic importance as they uncover the antidiuretic effect of β3-AR stimulation in the kidney. Hence, β3-AR agonism might be useful to bypass AVPR2-inactivating mutations.
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