ArticleAmerican journal of physiology. Renal physiology2011
Bradykinin acutely inhibits activity of the epithelial Na+ channel in mammalian aldosterone-sensitive distal nephron.
Article in American journal of physiology. Renal physiology, 2011. 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, 47 citations in OpenAlex.
- How Many Cell Types Are in the Kidney and What Do They Do?Annual review of physiology · 2022Review
- Biomarkers of Volume Overload and Edema in Heart Failure With Reduced Ejection Fraction.Frontiers in cardiovascular medicine · 2022Review
- Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises High KHypertension (Dallas, Tex. : 1979) · 2020Article
- Kir4.1/Kir5.1 in the DCT plays a role in the regulation of renal KAmerican journal of physiology. Renal physiology · 2019Article
- Bradykinin Stimulates Renal NaHypertension (Dallas, Tex. : 1979) · 2018Article
- Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac Hypertrophy.Frontiers in medicine · 2018Article
- Collecting duct prorenin receptor knockout reduces renal function, increases sodium excretion, and mitigates renal responses in ANG II-induced hypertensive mice.American journal of physiology. Renal physiology · 2017Article
- The renal TRPV4 channel is essential for adaptation to increased dietary potassium.Kidney international · 2017Article
- Functional and therapeutic importance of purinergic signaling in polycystic kidney disease.American journal of physiology. Renal physiology · 2016Review
- High salt diet and caffeine: food for thought.Journal of thoracic disease · 2016Article
- New insights into sodium transport regulation in the distal nephron: Role of G-protein coupled receptors.World journal of biological chemistry · 2016Review
- Neurophysiological mechanisms of bradykinin-evoked mucosal chloride secretion in guinea pig small intestine.World journal of gastrointestinal pathophysiology · 2016Article
- Insulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage.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
- Phosphoinositides regulate ion channels.Biochimica et biophysica acta · 2015Review
- Collecting duct principal cell transport processes and their regulation.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015Review
- Direct regulation of ENaC by bradykinin in the distal nephron. Implications for renal sodium handling.Current opinion in nephrology and hypertension · 2014Review
- Chronic angiotensin II infusion drives extensive aldosterone-independent epithelial Na+ channel activation.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Direct inhibition of basolateral Kir4.1/5.1 and Kir4.1 channels in the cortical collecting duct by dopamine.American journal of physiology. Renal physiology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Activation of the renal kallikrein-kinin system results in natriuresis and diuresis, suggesting its possible role in renal tubular sodium transport regulation. Here, we used patch-clamp electrophysiology to directly assess the effects of bradykinin (BK) on the epithelial Na(+) channel (ENaC) activity in freshly isolated split-opened murine aldosterone-sensitive distal nephrons (ASDNs). BK acutely inhibits ENaC activity by reducing channel open probability (P(o)) in a dose-dependent and reversible manner. Inhibition of B2 receptors with icatibant (HOE-140) abolished BK actions on ENaC. In contrast, activation of B1 receptors with the selective agonist Lys-des-Arg(9)-BK failed to reproduce BK actions on ENaC. This is consistent with B2 receptors playing a critical role in mediating BK signaling to ENaC. BK has little effect on ENaC P(o) when G(q/11) was inhibited with Gp antagonist 2A. Moreover, inhibition of phospholipase C (PLC) with U73122, but not saturation of cellular cAMP levels with the membrane-permeable nonhydrolysable cAMP analog 8-cpt-cAMP, prevents BK actions on ENaC activity. This argues that BK stimulates B2 receptors with subsequent activation of G(q/11)-PLC signaling cascade to acutely inhibit ENaC activity. Activation of BK signaling acutely depletes apical PI(4,5)P(2) levels. However, inhibition of Ca(2+) pump SERCA of the endoplasmic reticulum with thapsigargin does not prevent BK signaling to ENaC. Furthermore, caffeine, while producing a similar rise in [Ca(2+)](i) as in response to BK stimulation, fails to recapitulate BK actions on ENaC. Therefore, we concluded that BK acutely inhibits ENaC P(o) in mammalian ASDN via stimulation of B2 receptors and following depletion of PI(4,5)P(2), but not increases in [Ca(2+)](i).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.