ArticleThe Journal of clinical investigation2013
The absence of intrarenal ACE protects against hypertension.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed, 188 citations in OpenAlex.
- Effect of sodium bicarbonate supplementation on the renin-angiotensin system in patients with chronic kidney disease and acidosis: a randomized clinical trial.Journal of nephrology · 2021Trial
- Proximal tubule ACE2 mediates early responses to hypertension by regulating intrarenal RAS and sodium homeostasis.JCI insight · 2026Article
- Loss of OXGR1 function uncouples intrarenal RAS activation from pendrin and αENaC regulation and blunts angiotensin II-induced hypertension.Frontiers in pharmacology · 2026Article
- The relationship between estrogen and renin angiotensin system components in the context of hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Review
- Intercalated Cell ClC-K2 Channel Contributes to Systemic ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024Review
- Sex differences in renal transporters: assessment and functional consequences.Nature reviews. Nephrology · 2024Review
- Sex differences in blood pressure regulation and hypertension: renal, hemodynamic, and hormonal mechanisms.Physiological reviews · 2024Review
- Angiotensin II hypertension along the female rat tubule: predicted impact on coupled transport of NaAmerican journal of physiology. Renal physiology · 2023Article
- Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023Review
- A new immune disease: systemic hypertension.Clinical kidney journal · 2023Review
- Reactivity of renal and mesenteric resistance vessels to angiotensin II is mediated by NOXA1/NOX1 and superoxide signaling.American journal of physiology. Renal physiology · 2023Article
- Renal angiotensin I-converting enzyme-deficient mice are protected against aristolochic acid nephropathy.Pflugers Archiv : European journal of physiology · 2023Article
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- PPAR-α knockout leads to elevated blood pressure response to angiotensin II infusion associated with an increase in renal α-1 NaLife sciences · 2022Article
- Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension.Antioxidants & redox signaling · 2022Article
- NCC regulation by WNK signal cascade.Frontiers in physiology · 2022Review
- Characterization of pendrin in urinary extracellular vesicles in a rat model of aldosterone excess and in human primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- A five amino acids deletion in NKCC2 of C57BL/6 mice affects analysis of NKCC2 phosphorylation but does not impact kidney function.Acta physiologica (Oxford, England) · 2021Article
- Mutagenesis of the Cleavage Site of Pro Renin Receptor Abrogates Angiotensin II-Induced Hypertension in Mice.Hypertension (Dallas, Tex. : 1979) · 2021Article
61 more citing papers are in PubMed but not listed here.
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16 authors at 3 institutions in 1 country.
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Abstract
Activation of the intrarenal renin-angiotensin system (RAS) can elicit hypertension independently from the systemic RAS. However, the precise mechanisms by which intrarenal Ang II increases blood pressure have never been identified. To this end, we studied the responses of mice specifically lacking kidney angiotensin-converting enzyme (ACE) to experimental hypertension. Here, we show that the absence of kidney ACE substantially blunts the hypertension induced by Ang II infusion (a model of high serum Ang II) or by nitric oxide synthesis inhibition (a model of low serum Ang II). Moreover, the renal responses to high serum Ang II observed in wild-type mice, including intrarenal Ang II accumulation, sodium and water retention, and activation of ion transporters in the loop of Henle (NKCC2) and distal nephron (NCC, ENaC, and pendrin) as well as the transporter activating kinases SPAK and OSR1, were effectively prevented in mice that lack kidney ACE. These findings demonstrate that ACE metabolism plays a fundamental role in the responses of the kidney to hypertensive stimuli. In particular, renal ACE activity is required to increase local Ang II, to stimulate sodium transport in loop of Henle and the distal nephron, and to induce hypertension.
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