ArticleHypertension (Dallas, Tex. : 1979)2024
Role of Angiotensin II Type 1a Receptor (AT1aR) of Renal Tubules in Regulating Inwardly Rectifying Potassium Channels 4.2 (Kir4.2), Kir4.1, and Epithelial Na
Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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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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.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- New perspectives on thick ascending limb function and cell types.Kidney international · 2026Review
- Mechanistic target of rapamycin complex-1 plays a role in inhibiting kidney KAmerican journal of physiology. Renal physiology · 2026Article
- Mechanistic target of rapamycin complex-2 mediates the effect of overnight high KAmerican journal of physiology. Renal physiology · 2026Article
- Diet-Microbiota-Host Interactions in Regulation of Cardiometabolic Homeostasis: Emerging Mechanisms and Therapeutic Potential.Microbiota and host · 2025Article
- Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024Article
- Role of calcineurin in regulating renal potassium (KActa physiologica (Oxford, England) · 2024Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundKir4.2 and Kir4.1 play a role in regulating membrane transport in the proximal tubule (PT) and in the distal-convoluted-tubule (DCT), respectively.
methodsWe generated kidney-tubule-specific-AT1aR-knockout (Ks-AT1aR-KO) mice to examine whether renal AT1aR regulates Kir4.2 and Kir4.1.
resultsKs-AT1aR-KO mice had a lower systolic blood pressure than
conclusionsAT1aR determines the baseline membrane potential of PT by controlling Kir4.2 expression/activity but AT1aR is not required for determining the baseline membrane potential of the DCT and Kir4.1/Kir5.1 activity/expression. However, AT1aR is required for angiotensin II-induced hyperpolarization of basolateral membrane of PT and DCT. Deletion of AT1aR had no effect on baseline renal outer medullary potassium channel activity but increased ENaC activity in the CCD.
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Registered trials
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