ArticleHypertension (Dallas, Tex. : 1979)2009
Angiotensin II decreases nitric oxide synthase 3 expression via nitric oxide and superoxide in the thick ascending limb.
Article in Hypertension (Dallas, Tex. : 1979), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- 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
- Nephron-Specific Disruption of Nitric Oxide Synthase 3 Causes Hypertension and Impaired Salt Excretion.Journal of the American Heart Association · 2018Article
- A computational model for simulating solute transport and oxygen consumption along the nephrons.American journal of physiology. Renal physiology · 2016Article
- Angiotensin II-mediated hypertension impairs nitric oxide-induced NKCC2 inhibition in thick ascending limbs.American journal of physiology. Renal physiology · 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
- Angiotensin II-induced hypertension increases plasma membrane Na pump activity by enhancing Na entry in rat thick ascending limbs.American journal of physiology. Renal physiology · 2013Article
- Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4.American journal of physiology. Cell 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
- Luminal flow regulates NO and O2(-) along the nephron.American journal of physiology. Renal physiology · 2011Review
- 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
- Asymmetric dimethylarginine in angiotensin II-induced hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Nitric oxide reduces flow-induced superoxide production via cGMP-dependent protein kinase in thick ascending limbs.American journal of physiology. Renal physiology · 2009Article
Corrections and comments
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2 authors at 1 institution in 1 country.
Funding
Abstract
NO produced by NO synthase type 3 (NOS3) in medullary thick ascending limbs (mTHALs) inhibits Cl(-) reabsorption. Acutely, angiotensin II stimulates thick ascending limb NO production. In endothelial cells, NO inhibits NOS3 expression. Therefore, we hypothesized that angiotensin II decreases NOS3 expression via NO in mTHALs. After 24 hours, 10 and 100 nmol/L of angiotensin II decreased NOS3 expression by 23+/-9% (n=6; P<0.05) and 50+/-5% (n=7; P<0.001), respectively, in primary cultures of rat mTHALs. NO synthase inhibition by 4 mmol/L of N(G)-nitro-L-arginine methyl ester hydrochloride prevented angiotensin II from decreasing NOS3 expression (Delta=-5+/-8%; n=5). In the presence of N(G)-nitro-L-arginine methyl ester hydrochloride, the addition of exogenous NO (1 micromol/L spermine NONOate) restored the angiotensin II-induced decreases in NOS3 expression (-22+/-6%; n=7; P<0.013). In addition, NO scavenging with 10 micromol/L of carboxy-PTIO abolished the effect of angiotensin II in NOS3 expression (Delta=-1+/-8% versus carboxy-PTIO alone; n=6). Angiotensin II increases superoxide, and superoxide scavenges NO. Thus, we tested whether scavenging superoxide enhances the angiotensin II-induced reduction in NOS3 expression. Surprisingly, treatment with 100 micromol/L of Tempol, a superoxide dismutase mimetic, blocked the angiotensin II-induced decrease in NOS3 expression (Delta=-3+/-7%; n=6). This effect was not because of increased hydrogen peroxide. We concluded that angiotensin II-induced decreases in NOS3 expression in mTHALs require both NO and superoxide. Decreased NOS3 expression by angiotensin II in mTHALs could contribute to increased salt retention observed in angiotensin II-induced hypertension.
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