ArticleThe Journal of biological chemistry2010
Angiotensin II stimulates thick ascending limb NO production via AT(2) receptors and Akt1-dependent nitric-oxide synthase 3 (NOS3) activation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- The SRC/NF-κB-AKT/NOS3 axis as a key mediator of Kaempferol's protective effects against oxidative stress-induced osteoclastogenesis.Immunity, inflammation and disease · 2024Article
- The Angiotensin ATPharmacological reviews · 2022Review
- Angiotensin Type-2 Receptors: Transducers of Natriuresis in the Renal Proximal Tubule.International journal of molecular sciences · 2022Review
- Potential Effects of Bisphenol A on the Heart and Coronary Artery of Adult Male Rats and the Possible Role of L-Carnitine.Journal of toxicology · 2022Article
- Mechanisms of decreased tubular flow-induced nitric oxide in Dahl salt-sensitive rat thick ascending limbs.American journal of physiology. Renal physiology · 2021Article
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- Article
- Angiotensin II stimulates superoxide production by nitric oxide synthase in thick ascending limbs.Physiological reports · 2016Article
- 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
- TRPV4 activation mediates flow-induced nitric oxide production in the rat thick ascending limb.American journal of physiology. Renal physiology · 2014Article
- Iodinated contrast media cause direct tubular cell damage, leading to oxidative stress, low nitric oxide, and impairment of tubuloglomerular feedback.American journal of physiology. Renal physiology · 2014Article
- Oxidative stress in hypertension: role of the kidney.Antioxidants & redox signaling · 2014Review
- Role of angiotensin AT(2) receptors in natriuresis: Intrarenal mechanisms and therapeutic potential.Clinical and experimental pharmacology & physiology · 2013Review
- The intrarenal renin-angiotensin and dopaminergic systems: control of renal sodium excretion and blood pressure.Hypertension (Dallas, Tex. : 1979) · 2013Review
- Angiotensin-II-derived reactive oxygen species on baroreflex sensitivity during hypertension: new perspectives.Frontiers in physiology · 2013Article
- AT2 receptors: beneficial counter-regulatory role in cardiovascular and renal function.Pflugers Archiv : European journal of physiology · 2013Review
- 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
- ATP mediates flow-induced NO production in thick ascending limbs.American journal of physiology. Renal physiology · 2012Article
- Tumor necrosis factor α decreases nitric oxide synthase type 3 expression primarily via Rho/Rho kinase in the thick ascending limb.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Review article: the pathophysiological roles of the renin-angiotensin system in the gastrointestinal tract.Alimentary pharmacology & therapeutics · 2012Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Angiotensin II (Ang II) acutely stimulates thick ascending limb (TAL) NO via an unknown mechanism. In endothelial cells, activation of Ang II type 2 receptor (AT(2)) stimulates NO. Akt1 activates NOS3 by direct phosphorylation. We hypothesized that Ang II stimulates TAL NO production via AT(2)-mediated Akt1 activation, which phosphorylates NOS3 at serine 1177. We measured NO production by fluorescence microscopy. In isolated TALs, Ang II (100 nm) increased NO production by 1.1 +/- 0.2 fluorescence units/min (p < 0.01). Ang II increased cGMP accumulation by 4.9 +/- 1.3 fmol/microg (p < 0.01). Upon adding the AT(2) antagonist PD123319 (1 microm), Ang II failed to stimulate NO (0.1 +/- 0.1 fluorescence units/min; p < 0.001 versus Ang II); adding the AT(1) antagonist losartan (1 microm) resulted in Ang II stimulating NO by 0.9 +/- 0.1 fluorescence units/min. Akt inhibitor (5 microm) blocked Ang II-stimulated NO (-0.1 +/- 0.2 fluorescence units/min versus inhibitor alone). Phospho-Akt1 increased by 72% after 5 min (p < 0.006), returning to basal after 10 min. Phospho-Akt2 did not change after 5 min but increased by 115 and 163% after 10 and 15 min (p < 0.02). Phospho-Akt3 did not change. An AT(2) agonist increased pAkt1 by 78% (p < 0.02), PI3K inhibition blocked this effect. In TALs transduced with dominant negative Akt1, Ang II failed to stimulate NO (0.1 +/- 0.2 fluorescence units/min versus 1.2 +/- 0.2 for controls; p < 0.001). Ang II increased phospho-NOS3 at serine 1177 by 130% (p < 0.01) and 150% after 5 and 10 min (p < 0.02). Ang II increased phosphoNOS3 at serine 633 by 50% after 5 min (p < 0.01). Akt inhibition prevented NOS3 phosphorylation. We concluded that Ang II enhances TAL NO production via activation of AT(2) and Akt1-dependent phosphorylation of NOS3 at serines 1177 and 633.
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