Angiotensin II stimulates renal proximal tubule Na(+)-ATPase activity through the activation of protein kinase C |
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Authors: | Rangel L B A Caruso-Neves C Lara L S Lopes A G |
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Institution: | Departamento de Farmacologia Básica e Cli;nica, ICB, Universidade Federal do Rio de Janeiro, CCS-Bloco J, 21949-900, RJ, Rio de Janeiro, Brazil. |
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Abstract: | Recently, our group described an AT(1)-mediated direct stimulatory effect of angiotensin II (Ang II) on the Na(+)-ATPase activity of proximal tubules basolateral membranes (BLM) Am. J. Physiol. 248 (1985) F621]. Data in the present report suggest the participation of a protein kinase C (PKC) in the molecular mechanism of Ang II-mediated stimulation of the Na(+)-ATPase activity due to the following observations: (i) the stimulation of protein phosphorylation in BLM, induced by Ang II, is mimicked by the PKC activator TPA, and is completely reversed by the specific PKC inhibitor, calphostin C; (ii) the Na(+)-ATPase activity is stimulated by Ang II and TPA in the same magnitude, being these effects abolished by the use of the PKC inhibitors, calphostin C and sphingosine; (iii) the Na(+)-ATPase activity is activated by catalytic subunit of PKC (PKC-M), in a similar and nonadditive manner to Ang II; and (iv) Ang II stimulates the phosphorylation of MARCKS, a specific substrate for PKC. |
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