ArticleHypertension (Dallas, Tex. : 1979)2012
Angiotensin II type 2 receptor-mediated inhibition of NaCl absorption is blunted in thick ascending limbs from Dahl salt-sensitive rats.
Article in Hypertension (Dallas, Tex. : 1979), 2012. 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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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Regulatory effects of resveratrol on nitric oxide signaling in cardiovascular diseases.Pharmacological reports : PR · 2025Review
- Hypertonic Salt Solution Enhances Inflammatory Responses in Cultured Splenic T-Cells from Dahl Salt-Sensitive Rats but Not Dahl Salt-Resistant Rats.Journal of cardiovascular development and disease · 2023Article
- Effects of Angiotensin 1-7 and Mas Receptor Agonist on Renal System in a Rat Model of Heart Failure.International journal of molecular sciences · 2023Article
- Mechanisms of decreased tubular flow-induced nitric oxide in Dahl salt-sensitive rat thick ascending limbs.American journal of physiology. Renal physiology · 2021Article
- Maternal protein restriction induces renal AT2R promoter hypomethylation in salt-sensitive, hypertensive rats.Food science & nutrition · 2021Article
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- NADPH oxidase 4-derived superoxide mediates flow-stimulated NKCC2 activity in thick ascending limbs.American journal of physiology. Renal physiology · 2018Article
- Angiotensin AT2 receptor agonist prevents salt-sensitive hypertension in obese Zucker rats.American journal of physiology. Renal physiology · 2015Article
- 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
- Resveratrol increases nitric oxide production in the rat thick ascending limb via Ca2+/calmodulin.PloS one · 2014Article
- 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
- Role of angiotensin AT(2) receptors in natriuresis: Intrarenal mechanisms and therapeutic potential.Clinical and experimental pharmacology & physiology · 2013Review
- Epidermal growth factors in the kidney and relationship to hypertension.American journal of physiology. Renal physiology · 2013Review
- The intrarenal renin-angiotensin and dopaminergic systems: control of renal sodium excretion and blood pressure.Hypertension (Dallas, Tex. : 1979) · 2013Review
- AT2 receptors: beneficial counter-regulatory role in cardiovascular and renal function.Pflugers Archiv : European journal of physiology · 2013Review
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2 authors at 1 institution in 1 country.
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Abstract
NO reduces NaCl absorption by thick ascending limbs (TALs) by inhibiting the Na/K/2Cl cotransporter (NKCC2). We have shown that NO-induced inhibition of Na transport is reduced in Dahl salt-sensitive rat (SS) TALs. Angiotensin II increases NO production in TALs via angiotensin II type 2 receptor (AT(2)R). It is unknown whether AT(2)Rs regulate TAL NaCl absorption and whether this effect is reduced in SS rats. We hypothesized that AT(2)R activation decreases TAL Na transport via NO, and this effect is blunted in SS rats. In the presence of angiotensin II type 1 receptor antagonist losartan, AT(2)R activation with angiotensin II inhibited NKCC2 activity by 32±7% (P<0.03). AT(2)R antagonist PD-123319 abolished the effect of angiotensin II. Activation with the AT(2)R-selective agonist CGP42112A (10 nmol/L) decreased NKCC2 activity by 29±6% (P<0.03). The effect of CGP42112A on NKCC2 activity was blocked by PD-123319 and by NO synthase inhibitor N(G)-nitro-l-arginine methyl ester. In Dahl salt-resistant rat TALs, 1 nmol/L of CGP42112A decreased NKCC2 activity by 23±4% (P<0.01). In SS TALs, it had no effect. TAL AT(2)R mRNA did not differ in SS versus salt-resistant rats. We conclude the following: (1) TAL AT(2)R activation decreases Na absorption; (2) this effect is mediated by AT(2)R-induced stimulation of NO; (3) AT(2)R-induced reduction of NKCC2 activity is blunted in SS rats; and (4) defects in AT(2)R/NO signaling rather than decreased AT(2)R expression likely account for the blunted effect in SS TALs. Impaired AT(2)R-mediated signaling in TALs could contribute to the Na retention associated with salt-sensitive hypertension.
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