ArticlePhysiological genomics2015
Role of the Na+/H+ exchanger 3 in angiotensin II-induced hypertension.
Article in Physiological genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- A thermodynamically consistent approach to modeling epithelial solute and water transport in the proximal convoluted tubule.Journal of biological physics · 2026Article
- A traditional Korean fermented food,Heliyon · 2024Article
- Modelling hemodynamics regulation in rats and dogs to facilitate drugs safety risk assessment.Frontiers in pharmacology · 2024Article
- Gut microbiota dependant trimethylamine N-oxide and hypertension.Frontiers in physiology · 2023Review
- Genetic Deletion of ATInternational journal of molecular sciences · 2022Article
- The Post-Translational Modification Networking in WNK-Centric Hypertension Regulation and Electrolyte Homeostasis.Biomedicines · 2022Review
- Intestinal Gastrin/CCKBR (Cholecystokinin B Receptor) Ameliorates Salt-Sensitive Hypertension by Inhibiting Intestinal NaHypertension (Dallas, Tex. : 1979) · 2022Article
- A modular and reusable model of epithelial transport in the proximal convoluted tubule.PloS one · 2022Review
- The NaFrontiers in physiology · 2022Review
- Sex differences in angiotensin II-induced hypertension and kidney injury: role of AT1a receptors in the proximal tubule of the kidney.Clinical science (London, England : 1979) · 2021Article
- New Insights into the Critical Importance of Intratubular NaCurrent hypertension reports · 2021Review
- Proximal Tubule-Specific Deletion of Angiotensin II Type 1a Receptors in the Kidney Attenuates Circulating and Intratubular Angiotensin II-Induced Hypertension in PT-Hypertension (Dallas, Tex. : 1979) · 2021Article
- Intratubular, Intracellular, and Mitochondrial Angiotensin II/ATFrontiers in physiology · 2021Review
- Dietary fructose enhances angiotensin II-stimulated NaAmerican journal of physiology. Renal physiology · 2020Article
- Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Proximal Tubule-Specific Deletion of the NHE3 (NaHypertension (Dallas, Tex. : 1979) · 2019Article
- Genetic and genomic evidence for an important role of the NaPhysiological genomics · 2019Review
- Proximal Tubule-Specific Deletion of the NHE3 (NaHypertension (Dallas, Tex. : 1979) · 2018Article
- Simultaneous GLP-1 receptor activation and angiotensin receptor blockade increase natriuresis independent of altered arterial pressure in obese OLETF rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The renal mechanisms responsible for angiotensin II (ANG II)-induced hypertension remain incompletely understood. The present study tested the hypothesis that the Na(+)/H(+) exchanger 3 (NHE3) is required for ANG II-induced hypertension in mice. Five groups of wild-type (Nhe3(+/+)) and Nhe3(-/-) mice were treated with vehicle or high pressor doses of ANG II (1.5 mg/kg/day ip, via minipump for 2 wk, or 10 pmol/min iv for 30 min). Under basal conditions, Nhe3(-/-) mice had significantly lower systolic blood pressure (SBP) and mean intra-arterial pressure (MAP) (P < 0.01), 24 h urine (P < 0.05), urinary Na(+) (P < 0.01) and urinary K(+) excretion (P < 0.01). In response to ANG II, SBP and MAP markedly increased in Nhe3(+/+) mice in a time-dependent manner, as expected (P < 0.01). However, these acute and chronic pressor responses to ANG II were significantly attenuated in Nhe3(-/-) mice (P < 0.01). Losartan blocked ANG II-induced hypertension in Nhe3(+/+) mice but induced marked mortality in Nhe3(-/-) mice. The attenuated pressor responses to ANG II in Nhe3(-/-) mice were associated with marked compensatory humoral and renal responses to genetic loss of intestinal and renal NHE3. These include elevated basal plasma ANG II and aldosterone and kidney ANG II levels, salt wasting from the intestines, increased renal AQP1, Na(+)/HCO3 (-), and Na(+)/K(+)-ATPase expression, and increased PKCα, mitogen-activated protein kinases ERK1/2, and glycogen synthase kinase 3αβ signaling proteins in the proximal tubules (P < 0.01). We concluded that NHE3 in proximal tubules of the kidney, along with NHE3 in intestines, is required for maintaining basal blood pressure as well as the full development of ANG II-induced hypertension.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.