Impaired Stimulatory Effect of ETB Receptor on D3 Receptor in Immortalized Renal Proximal Tubule Cells of Spontaneously Hypertensive Rats
Year: 2011
Type: article
Abstract: BACKGROUND: Activation of renal D₃ receptor induces natriuresis and diuresis in Wistar-Kyoto (WKY) rats; in the presence of ETB receptor antagonist, the natriuretic effect of D₃ receptor in WKY rats is reduced. We hypothesize that ETB receptor activation may regulate D₃ receptor expression in renal proximal tubule (RPT) cells from WKY rats, which is impaired in RPT cells from spontaneously hypertensive rats (SHRs). METHODS: D₃ receptor expression was determined by immunoblotting; the D₃/ETB receptor linkage was checked by coimmunoprecipitation; Na(+)-K(+)-ATPase activity was determined as the rate of inorganic phosphate released in the presence or absence of ouabain. RESULTS: In RPT cells from WKY rats, the ETB receptor agonist BQ3020 increased D₃ receptor protein. In contrast, in RPT cells from SHRs, BQ3020 did not increase D₃ receptor. There was coimmunoprecipitation between D₃ and ETB receptors in RPT cells from WKY and SHRs. Activation of ETB receptor increased D₃/ETB coimmunoprecipitation in RPT cells from WKY rats, but not from SHRs. The basal levels of D₃/ETB receptor coimmunoprecipitation were greater in RPT cells from WKY rats than in those from SHRs. Stimulation of D₃ receptor inhibited Na(+)-K(+)-ATPase activity, which was augmented by the pretreatment with the ETB receptor agonist BQ3020 in WKY RPT cells, but not in SHR RPT cells. CONCLUSION: ETB receptors regulate and physically interact with D₃ receptors differently in WKY rats and SHRs. The impaired natriuretic effect in SHRs may be, in part, related to impaired ETB and D₃ receptor interactions.
Source: Kidney & Blood Pressure Research
DOI: 10.1159/000323135
Authors: Ye Zhang, Chunjiang Fu, Hongmei Ren, Duofen He, Xukai Wang, Laureano D. Asico, Pedro A. Jose, Chunyu Zeng
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Funders: National Natural Science Foundation of China, Chongqing Science and Technology Commission, Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission, National Institutes of Health, National Key Research and Development Program of China, National Heart, Lung, and Blood Institute, National Institute of Diabetes and Digestive and Kidney Diseases
Awards: G1064172643, G1403022750, G1787520283, Molecular Mechanisms in Salt Sensitivity of Blood Pressure, G1828425977, G2038307099, G2171017283, G蛋白激酶4变异体A486V在高血压病肾脏多巴胺D3受体功能障碍中的作用研究, GRK4变异体A142V对原发性高血压肾脏AT1受体调控的机制, G4091823529, G4336536781, Renal dopamine-1 receptor defect in hypertension, G572264085, G5935051251, Oxidative Stress In The Kidney In Hypertension, Renal Dopamine Receptor and Regulation, GRK4 & Development of Salt Sensitivity, G9000062685, G9000176767, G9000349341
OpenAlex ID: W2088159883
