ArticleJournal of the American Society of Nephrology : JASN2014
Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 52 citations in OpenAlex.
- HIV-Associated Hypertension: Risks, Mechanisms, and Knowledge Gaps.Circulation research · 2024Review
- Endothelial Nitric Oxide synthase (eNOS) in Preeclampsia: An Update.Journal of pregnancy and child health · 2024Article
- Measured GFR in murine animal models: review on methods, techniques, and procedures.Pflugers Archiv : European journal of physiology · 2023Review
- Renal angiotensin I-converting enzyme-deficient mice are protected against aristolochic acid nephropathy.Pflugers Archiv : European journal of physiology · 2023Article
- Methods for Assessment of the Glomerular Filtration Rate in Laboratory Animals.Kidney diseases (Basel, Switzerland) · 2022Review
- Endothelial leptin receptor is dispensable for leptin-induced sympatho-activation and hypertension in male mice.Vascular pharmacology · 2022Article
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- Hypertension and human immunodeficiency virus: A paradigm for epithelial sodium channels?Frontiers in cardiovascular medicine · 2022Review
- Novel roles of the renal angiotensin-converting enzyme.Molecular and cellular endocrinology · 2021Review
- Article
- Chronic L-Name-Treatment Produces Hypertension by Different Mechanisms in Peripheral Tissues and Brain: Role of Central eNOS.Pathophysiology : the official journal of the International Society for Pathophysiology · 2020Article
- Kidney-specific lymphangiogenesis increases sodium excretion and lowers blood pressure in mice.Journal of hypertension · 2020Article
- Low Nitric Oxide Bioavailability Increases Renin Production in the Collecting Duct.Frontiers in physiology · 2020Article
- Beneficial effects of nicotinamide on hypertensive mice with impaired endothelial nitric oxide function.Journal of experimental nephrology · 2020Article
- The Effects of Irisin on Nω-Nitro-L-arginine Methyl Ester Hydrochloride-Induced Hypertension in RatsBalkan medical journal · 2019Article
- Podocyte Injury Augments Intrarenal Angiotensin II Generation and Sodium Retention in a Megalin-Dependent Manner.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Antihypertensive effects of the hydro-ethanol extract of Senecio serratuloides DC in rats.BMC complementary and alternative medicine · 2019Article
- The Absence of the ACE N-Domain Decreases Renal Inflammation and Facilitates Sodium Excretion during Diabetic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Renal tubular ACE-mediated tubular injury is the major contributor to microalbuminuria in early diabetic nephropathy.American journal of physiology. Renal physiology · 2018Article
- Collecting Duct Nitric Oxide Synthase 1ß Activation Maintains Sodium Homeostasis During High Sodium Intake Through Suppression of Aldosterone and Renal Angiotensin II Pathways.Journal of the American Heart Association · 2017Article
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13 authors at 6 institutions in 2 countries.
Funding
Abstract
The kidney is an important source of angiotensin-converting enzyme (ACE) in many species, including humans. However, the specific effects of local ACE on renal function and, by extension, BP control are not completely understood. We previously showed that mice lacking renal ACE, are resistant to the hypertension induced by angiotensin II infusion. Here, we examined the responses of these mice to the low-systemic angiotensin II hypertensive model of nitric oxide synthesis inhibition with L-NAME. In contrast to wild-type mice, mice without renal ACE did not develop hypertension, had lower renal angiotensin II levels, and enhanced natriuresis in response to L-NAME. During L-NAME treatment, the absence of renal ACE was associated with blunted GFR responses; greater reductions in abundance of proximal tubule Na(+)/H(+) exchanger 3, Na(+)/Pi co-transporter 2, phosphorylated Na(+)/K(+)/Cl(-) cotransporter, and phosphorylated Na(+)/Cl(-) cotransporter; and greater reductions in abundance and processing of the γ isoform of the epithelial Na(+) channel. In summary, the presence of ACE in renal tissue facilitates angiotensin II accumulation, GFR reductions, and changes in the expression levels and post-translational modification of sodium transporters that are obligatory for sodium retention and hypertension in response to nitric oxide synthesis inhibition.
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