ArticleAmerican journal of hypertension2015
Enhanced Natriuresis and Diuresis in Wistar Rats Caused by the Costimulation of Renal Dopamine D3 and Angiotensin II Type 2 Receptors.
Article in American journal of hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Dopamine Receptor DThe Yale journal of biology and medicine · 2023Review
- The Angiotensin ATPharmacological reviews · 2022Review
- Inverse Salt Sensitivity of Blood Pressure: Mechanisms and Potential Relevance for Prevention of Cardiovascular Disease.Current hypertension reports · 2022Review
- G-protein-coupled receptor kinase 4 causes renal angiotensin II type 2 receptor dysfunction by increasing its phosphorylation.Clinical science (London, England : 1979) · 2022Article
- Angiotensin Type-2 Receptors: Transducers of Natriuresis in the Renal Proximal Tubule.International journal of molecular sciences · 2022Review
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- The Role of the Renal Dopaminergic System and Oxidative Stress in the Pathogenesis of Hypertension.Biomedicines · 2021Review
- GRK4-mediated adiponectin receptor-1 phosphorylative desensitization as a novel mechanism of reduced renal sodium excretion in hypertension.Clinical science (London, England : 1979) · 2020Article
- Update on angiotensin AT2 receptors.Current opinion in nephrology and hypertension · 2017Review
- Downregulation of Renal G Protein-Coupled Receptor Kinase Type 4 Expression via Ultrasound-Targeted Microbubble Destruction Lowers Blood Pressure in Spontaneously Hypertensive Rats.Journal of the American Heart Association · 2016Article
- Kidney tubules: intertubular, vascular, and glomerular cross-talk.Current opinion in nephrology and hypertension · 2016Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe kidney, via its regulation of sodium excretion, which is modulated by humoral factors, including the dopamine and renin-angiotensin systems, keeps the blood pressure in the normal range. We have reported a negative interaction between dopamine D3 and AT1 receptors (D3R and AT1R) in renal proximal tubule (RPT) cells. Here, we studied the interaction between D3R and AT2R in vitro and in vivo. METHODS AND
resultsStimulation of either the D3R or AT2R, by the intrarenal arterial infusion of PD128907, a D3R agonist, or CGP42112A, an AT2R agonist, induced natriuresis and diuresis that were enhanced by the simultaneous infusion of PD128907 and CGP42112A in Wistar rats. The D3/AT2 receptor interaction was confirmed in in vitro, i.e., stimulation of either the D3R or AT2R inhibited Na(+)-K(+)-ATPase activity that was enhanced by the costimulation of these receptors. D3R and AT2R colocalized and coimmunoprecipitated in kidney and RPT cells (RPTCs). Stimulation of one receptor increased the localization of the other receptor at the plasma cell membrane. ERK1/2-MAPK is involved in the signaling pathway of D3R and AT2R interaction because costimulation of D3R and AT2R significantly increased ERK1/2-MAPK expression in RPTCs; inhibition of ERK1/2-MAPK abolished the inhibition of Na(+)-K(+)-ATPase activity that was enhanced by D3R and AT2R costimulation.
conclusionsOur current study indicates that D3R, in combination with AT2R, enhances natriuresis and diuresis, via ERK1/2-MAPK pathway, that may be involved in the regulation of blood pressure.
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