ReviewCurrent opinion in nephrology and hypertension2014
Direct regulation of ENaC by bradykinin in the distal nephron. Implications for renal sodium handling.
Review in Current opinion in nephrology and hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- (Pro)renin Receptor Blockade Prevents Increases in Systolic Blood Pressure, Sodium Retention, and αENaC Protein Expression in the Kidney of 2K1C Goldblatt Mice.International journal of molecular sciences · 2025Article
- Review
- Biomarkers of Volume Overload and Edema in Heart Failure With Reduced Ejection Fraction.Frontiers in cardiovascular medicine · 2022Review
- Urinary proteomics reveals key markers of salt sensitivity in hypertensive patients during saline infusion.Journal of nephrology · 2021Article
- Hypothetical dysfunction of the epithelial sodium channel may justify neurohumoral blockade in coronavirus disease 2019.ESC heart failure · 2021Article
- Diurnal Regulation of Renal Electrolyte Excretion: The Role of Paracrine Factors.Annual review of physiology · 2020Review
- A Pathophysiological Model for COVID-19: Critical Importance of Transepithelial Sodium Transport upon Airway Infection.Function (Oxford, England) · 2020Article
- The promise of zebrafish as a model of metabolic syndrome.Experimental animals · 2019Review
- Evidence against a crucial role of renal medullary perfusion in blood pressure control of hypertensive rats.The Journal of physiology · 2019Article
- Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac Hypertrophy.Frontiers in medicine · 2018Article
- Kidney tubules: intertubular, vascular, and glomerular cross-talk.Current opinion in nephrology and hypertension · 2016Review
- New insights into sodium transport regulation in the distal nephron: Role of G-protein coupled receptors.World journal of biological chemistry · 2016Review
- Vasopressin/V2 receptor stimulates renin synthesis in the collecting duct.American journal of physiology. Renal physiology · 2016Article
- Conditional knockout of collecting duct bradykinin B2 receptors exacerbates angiotensin II-induced hypertension during high salt intake.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2016Article
- Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewLocally produced peptide hormones kinins, such as bradykinin, are thought to oppose many of the prohypertensive actions of the renin-angiotensin-aldosterone system. In the kidney, bradykinin, via stimulation of B2 receptors (B2R), favors natriuresis mostly due to the inhibition of tubular Na reabsorption. Recent experimental evidence identifies the epithelial Na channel (ENaC) as a key end effector of bradykinin actions in the distal tubular segments. The focus of this review is the physiological relevance and molecular details of the bradykinin signal to ENaC. RECENT
findingsThe recent epidemiological GenSalt study demonstrated that genetic variants of the gene encoding B2R show significant associations with the salt sensitivity of blood pressure. Bradykinin was shown to have an inhibitory effect on the distal nephron sodium transport via stimulation of B2 receptor-phospholipase C (B2R-PLC) cascade to decrease ENaC open probability. Genetic ablation of bradykinin receptors in mice led to an augmented ENaC function, particularly during elevated sodium intake, likely contributing to the salt-sensitive hypertensive phenotype. Furthermore, augmentation of bradykinin signaling in the distal nephron was demonstrated to be an important component of the natriuretic and antihypertensive effects of angiotensin converting enzyme inhibition. SUMMARY: Salt-sensitive inhibition of ENaC activity by bradykinin greatly advances our understanding of the molecular mechanisms that are responsible for shutting down distal tubule sodium reabsorption during volume expanded conditions to avoid salt-sensitive hypertension.
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