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• W4377029498 abstract "<b>Abstract ID 21314</b> <b>Poster Board 110</b> Our previous studies have demonstrated that sphingosine-1-phosphate (S1P) agonist stimulates urinary sodium excretion via the S1P type 1 receptor (S1PR1), that deletion of S1PR1 gene in the renal collecting duct leads to increased sodium retention and enhanced salt-sensitive hypertension under the treatment of deoxycorticosterone (DOCA) and high salt (DOCA-salt), and further, that overexpression of S1PR1 transgene in the renal medulla attenuates DOCA-salt hypertension. A pharmacological intervention would bear more clinical implications. Therefore, the present study tested the hypothesis that oral administration of a selective S1PR agonist BAF312 reduces sodium retention by promoting sodium excretion and consequently attenuates DOCA-salt hypertension. Male C57BL/6J mice around 25g bodyweight received daily oral gavage of BAF312 (3 mg/Kg dissolved in PEG-400) or vehicle for one week. The mice were then implanted subcutaneously with a silicone sheet (silastic, Dow Corning Co.) impregnated with DOCA (50mg each mouse) plus 1% NaCl drinking water to induce salt-sensitive hypertension. Thereafter, the mice underwent assessments of acute sodium excretion, chronic sodium balance or chronic blood pressure measurement. There was no difference in the above assessments between vehicle- and BAF312-treated mice under basal conditions. Under DOCA-salt challenge, mice with BAF312 treatment showed increased urinary sodium excretion (U_NAV) in responses to the acute sodium loading (IV of normal saline at 5% body weight in 30 min), the U_NAV were 1.85±0.22 vs. 5.81±1.14 μmol/min/gKW (p<0.05) in vehicle- and BAF312-treated mice, respectively. The mice with BAF312 treatment also showed enhanced pressure natriuretic responses to the elevated renal perfusion pressure (U_NAV, 4.24±1.14 vs. 13.3±1.57 μmol/min/gKW, in vehicle- and BAF312-treated mice, respectively, p<0.05). Under the chronic DOCA-salt treatment, BAF312-treated mice showed ameliorated sodium retention as demonstrated by the less positive sodium balance (4.78±0.38 vs. 1.23±1.18 mmol/100g BW per 24hr in vehicle- vs. BAF312-treated mice, p<0.05) and the attenuation of increased blood pressure after 10-day DOCA-salt treatment, the systolic blood pressure were increased from 119±5.3 to 156.2±9.7 vs. 119±6.9 to 133.8±7.5mmHg in vehicle- and BAF312-treated mice, respectively (p<0.05). These results suggested that oral administration of the selective S1PR1 agonist BAF312 attenuates sodium retention and DOCA-induced salt-sensitive hypertension and that BAF312 could be a pharmacological candidate for the management of salt-sensitive hypertension. This study was supported by NIH grant R01HL145163" @default.
• W4377029498 created "2023-05-19" @default.
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• W4377029498 date "2023-05-18" @default.
• W4377029498 modified "2023-09-29" @default.
• W4377029498 title "Oral administration of BAF312, a selective sphingosine-1-phosphate receptor agonist, attenuates sodium retention and hypertension in DOCA-salt-treated mice" @default.
• W4377029498 doi "https://doi.org/10.1124/jpet.122.213140" @default.
• W4377029498 hasPublicationYear "2023" @default.
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