ArticleAmerican journal of physiology. Renal physiology2015
Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Early-life sodium restriction programs autonomic dysfunction and salt sensitivity in male C57BL/6J mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Sodium Chloride Cotransporter in Hypertension.Biomedicines · 2024Review
- Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024Article
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron.American journal of physiology. Cell physiology · 2022Article
- Deletion of Kir5.1 abolishes the effect of high NaAmerican journal of physiology. Renal physiology · 2021Article
- Rapid Aldosterone-Mediated Signaling in the DCT Increases Activity of the Thiazide-Sensitive NaCl Cotransporter.Journal of the American Society of Nephrology : JASN · 2019Article
- The interplay of renal potassium and sodium handling in blood pressure regulation: critical role of the WNK-SPAK-NCC pathway.Journal of human hypertension · 2019Review
- Zebrafish as a Model System for Investigating the Compensatory Regulation of Ionic Balance during Metabolic Acidosis.International journal of molecular sciences · 2018Review
- Characterization of constitutive and acid-induced outwardly rectifying chloride currents in immortalized mouse distal tubular cells.Biochimica et biophysica acta. General subjects · 2017Article
- WNK signalling pathways in blood pressure regulation.Cellular and molecular life sciences : CMLS · 2017Review
- Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Hypertension: the missing WNKs.American journal of physiology. Renal physiology · 2016Review
- A novel function of calcitonin gene-related peptide in body fluid Cl- homeostasis.Proceedings. Biological sciences · 2016Article
- Regulatory Crosstalk by Protein Kinases on CFTR Trafficking and Activity.Frontiers in chemistry · 2016Review
- Short-term nonpressor angiotensin II infusion stimulates sodium transporters in proximal tubule and distal nephron.Physiological reports · 2015Article
- Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.American journal of physiology. Cell physiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Angiotensin II (ANG II) increases thiazide-sensitive sodium-chloride cotransporter (NCC) activity both acutely and chronically. ANG II has been implicated as a switch that turns WNK4 from an inhibitor of NCC into an activator of NCC, and ANG II's effect on NCC appears to require WNK4. Chronically, ANG II stimulation of NCC results in an increase in total and phosphorylated NCC, but the role of NCC phosphorylation in acute ANG II actions is unclear. Here, using a mammalian cell model with robust native NCC activity, we corroborate the role that ANG II plays in WNK4 regulation and clarify the role of Ste20-related proline alanine-rich kinase (SPAK)-induced NCC phosphorylation in ANG II action. ANG II was noted to have a biphasic effect on NCC, with a peak increase in NCC activity in the physiologic range of 10(-11) M ANG II. This effect was apparent as early as 15 min and remained sustained through 120 min. These changes correlated with significant increases in NCC surface protein expression. Knockdown of WNK4 expression sharply attenuated the effect of ANG II. SPAK knockdown did not affect ANG II action at early time points (15 and 30 min), but it did attenuate the response at 60 min. Correspondingly, NCC phosphorylation did not increase at 15 or 30 min, but increased significantly at 60 min. We therefore conclude that within minutes of an increase in ANG II, NCC is rapidly trafficked to the cell surface in a phosphorylation-independent but WNK4-dependent manner. Then, after 60 min, ANG II induces SPAK-dependent phosphorylation of NCC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.