PKA-mediated effect of MAS receptor in counteracting angiotensin II-stimulated renal Na-ATPase |
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Authors: | Lucienne S Lara Juliana S Correa Maria Fernanda Marques-Fernades Celso Caruso-Neves |
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Institution: | a Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, CCS-bloco J, 21941-590, Rio de Janeiro, RJ, Brazil b Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS-bloco G, 21941-902, Rio de Janeiro, RJ, Brazil c Instituto Nacional de Ciência e Tecnologia em Biologia Estrutural e Bioimagem (INBEB), Rio de Janeiro, RJ, Brazil |
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Abstract: | We showed previously that angiotensin-(1-7) Ang-(1-7)] reversed stimulation of proximal tubule Na+-ATPase promoted by angiotensin II (Ang II) through a d-ala7-Ang-(1-7) (A779)-sensitive receptor. Here we investigated the signaling pathway coupled to this receptor. According to our data, Ang-(1-7) produces a MAS-mediated reversal of Ang II-stimulated Na+-ATPase by a Gs/PKA pathway because: (1) the Ang-(1-7) effect is reversed by GDPβS, an inhibitor of trimeric G protein and Gs polyclonal antibody. Cholera toxin, an activator of Gs protein, mimicked it; (2) in the presence of Ang II, Ang-(1-7) increased the PKA activity 10-fold; (3) the peptide inhibitor of PKA blocked the Ang-(1-7) effect on Ang II-stimulated Na+-ATPase; (4) Ang-(1-7) reverses the Ang II-stimulated PKC activity; (5) cAMP mimicked the Ang-(1-7) effect on the Ang II-stimulated Na+-ATPase. Our results provide new understanding about the signaling mechanisms coupled to MAS receptor-mediated renal Ang-(1-7) effects. |
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Keywords: | Renal sodium excretion MAS receptor signaling Second sodium pump Angiotensin II Angiotensin-(1-7) |
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