Angiotensin II stimulates renal proximal tubule Na(+)-ATPase activity through the activation of protein kinase C.
Biochim Biophys Acta
; 1564(2): 310-6, 2002 Aug 31.
Article
en En
| MEDLINE
| ID: mdl-12175912
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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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteína Quinasa C
/
Angiotensina II
/
Adenosina Trifosfatasas
/
Proteínas de Transporte de Catión
/
Túbulos Renales Proximales
Límite:
Animals
Idioma:
En
Revista:
Biochim Biophys Acta
Año:
2002
Tipo del documento:
Article
País de afiliación:
Brasil
Pais de publicación:
Países Bajos