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• W2048089340 endingPage "226" @default.
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• W2048089340 abstract "In the present paper the effect of Ang-(1–7) on the distal tubule (Na+ + K+)ATPase activity was evaluated by using MDCK cells as a model. Confluent cell monolayers were incubated with increasing concentrations of Ang-(1–7) for 30 min. Thereafter, the (Na+ + K+)ATPase activity was evaluated and a dose–dependent (from 10−12 to 10−7 M) inhibition was observed. The maximal inhibitory effect (54%) was reached at the concentration of 10−8 M. The inhibitory effect of Ang-(1–7) was not affected by the AT2 receptor selective antagonist PD123319 (from 10−10 to 10−7 M) but was blocked in a dose–dependent manner by the AT1 receptor selective antagonists losartan (10−10 M), candesartan (10−17 M), irbesartan (2 × 10−12 M) and telmisartan (2 × 10−16 M). The signaling pathway triggered by stimulation of the AT1 receptor was also investigated. The PI-phospholipase C (PI-PLC) inhibitor U73122 (5 × 10−8 M) blocked the inhibitory effect elicited by Ang-(1–7). Involvement of the protein kinase C (PKC) was evidenced by the sensitivity of the inhibitory effect of Ang-(1–7) to calphostin C (6.32 × 10−7 M) and the lack of additive effects when the cells were co-incubated with Ang-(1–7) and 3.2 × 10−8 M PMA. Altogether, these results demonstrate that Ang-(1–7) inhibits the (Na+ + K+)ATPase activity of the prototypic distal tubule cell MDCK through the AT1 receptor-mediated stimulation of PI-PLC/PKC signaling pathway." @default.
• W2048089340 created "2016-06-24" @default.
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• W2048089340 date "2005-07-01" @default.
• W2048089340 modified "2023-09-23" @default.
• W2048089340 title "Modulation of the (Na++K+)ATPase activity by Angiotensin-(1–7) in MDCK cells" @default.
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• W2048089340 doi "https://doi.org/10.1016/j.regpep.2005.02.014" @default.
• W2048089340 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15927719" @default.
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