ArticleAmerican journal of physiology. Renal physiology2009
Akt1 mediates purinergic-dependent NOS3 activation in thick ascending limbs.
Article in American journal of physiology. Renal physiology, 2009. 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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15 citing papers in PubMed, 19 citations in OpenAlex.
- Epigenome-wide association studies of meat traits in Chinese Yorkshire pigs highlights several DNA methylation loci and genes.Frontiers in genetics · 2022Article
- A Computational Exploration of the Molecular Network Associated to Neuroinflammation in Alzheimer's Disease.Frontiers in pharmacology · 2021Article
- P2Y2R contributes to the development of diabetic nephropathy by inhibiting autophagy response.Molecular metabolism · 2020Article
- Angiotensin-(1-7) inhibits sodium transport via Mas receptor by increasing nitric oxide production in thick ascending limb.Physiological reports · 2019Article
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- Angiotensin II-induced hypertension blunts thick ascending limb NO production by reducing NO synthase 3 expression and enhancing threonine 495 phosphorylation.American journal of physiology. Renal physiology · 2015Article
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- Distinct regulation of inner medullary collecting duct nitric oxide production from mice and rats.Clinical and experimental pharmacology & physiology · 2013Article
- NADPH oxidase 4 mediates flow-induced superoxide production in thick ascending limbs.American journal of physiology. Renal physiology · 2012Article
- Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4.American journal of physiology. Cell physiology · 2012Article
- Angiotensin II type 2 receptor-mediated inhibition of NaCl absorption is blunted in thick ascending limbs from Dahl salt-sensitive rats.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Nitric oxide synthase 3 deficiency limits adverse ventricular remodeling after pressure overload in insulin resistance.American journal of physiology. Heart and circulatory physiology · 2011Article
- Angiotensin II stimulates thick ascending limb NO production via AT(2) receptors and Akt1-dependent nitric-oxide synthase 3 (NOS3) activation.The Journal of biological chemistry · 2010Article
- Rac1 mediates NaCl-induced superoxide generation in the thick ascending limb.American journal of physiology. Renal physiology · 2010Article
- Extracellular ATP inhibits transport in medullary thick ascending limbs: role of P2X receptors.American journal of physiology. Renal physiology · 2009Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular ATP regulates many physiological processes via release of nitric oxide (NO). ATP stimulates NO in thick ascending limbs (TALs), but the signaling cascade involved in the cells of this nephron segment, as well as many other types of cells, is poorly understood. We hypothesized that ATP enhances NO synthase (NOS) activity by stimulating PI3 kinase and Akt. We measured 1) NO in TALs using the NO-sensitive dye DAF-2 DA and 2) Akt activity by fluorescence resonance energy transfer and phosphorylation of Akt isoforms. ATP (100 microM) stimulated NO in wild-type mice [26 +/- 4 arbitrary units (AU)], but not in NOS3 -/- mice (2 +/- 2 AU; P < 0.04). In the presence of the NOS1- and NOS2-selective inhibitors 7-NI and 1400W, ATP stimulated NO by 30 +/- 2 and 33 +/- 3 AU, respectively (not significant vs. control). In the presence of the PI3 kinase inhibitor LY294002, ATP-increased NO was reduced by 85% (5 +/- 2 vs. 28 +/- 4 AU; P < 0.02). ATP alone increased Akt activity and this effect was significantly blocked by suramin, a P2 receptor antagonist. In the presence of an Akt-selective inhibitor, ATP-induced NO was blocked by 90 +/- 4%. ATP significantly stimulated Akt1 phosphorylation at Ser(473) by 91 +/- 13%, whereas Akt2 phosphorylation remained unchanged and Akt3 phosphorylation decreased. In vivo transduction of TALs with a dominant-negative Akt1 significantly decreased ATP-induced NO by 88 +/- 6%. We concluded that ATP increases NOS3-derived NO via Akt1 activation in the TAL.
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