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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Signaling path of the action of AVP on distal K+ secretion

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Autor(es):
Amorim, José B. O. ; Musa-Aziz, Raif ; Mello-Aires, Margarida ; Malnic, Gerhard [4]
Número total de Autores: 4
Tipo de documento: Artigo Científico
Fonte: Kidney International; v. 66, n. 2, p. 696-704, Aug. 2004.
Área do conhecimento: Ciências Biológicas - Fisiologia
Assunto(s):Túbulos renais distais   Canais de potássio   Proteína quinase C   Estaurosporina
Resumo

Previous studies from our laboratory have shown that luminal perfusion with arginine vasopressin (AVP) stimulates distal tubule secretory potassium flux (JK) via V1 receptors (Am J Physiol 278:F809-F816, 2000). In the present work, we investigate the cell signaling mechanism of thisprocess. In vivo stationary microperfusion was performed in rat cortical distal tubules and luminal K+ was measured using double K+ resin/reference microelectrodes. In control conditions, JK was 0.71 0.05 nmol. cm-2.second-1; this process was inhibited (14%) by 10-5 mol/L 8-bromo-cyclic adenosine monophosphate (cAMP), and increased by 35% with 10-8 mol/L phorbol ester [phorbol12-myristate 13-acetate (PMA), which activates protein kinase C (PKC)]. During luminal perfusion with 10-11 mol/L AVP, JK increased to 0.88 0.08 nmol.cm-2.seconds-1. In the presence of 10-11 mol/L AVP, JK was not affected by 10-4 mol/L H89, a blocker of protein kinase A (PKA), but was inhibited (45%) by 10-5 mol/L staurosporine, an inhibitor of PKC, and by 41% during perfusion with 5 10-5 mol/L of the cell Ca2+ chelator bis (2-aminophenoxy) ethane-tetraacetic acid (BAPTA). In order to study the role of Ca2+-dependent K channels in the luminal hormonal action, the tubules were perfused with 5 mmol/L tetraethylammonium chloride (TEA) or 10-7 mol/L iberiotoxin, in the presence of AVP, and JK was significantly reduced by both agents. Iberiotoxin reduced AVP-stimulated JK by 36.4%, and AVP-independent JK (after blocking V1 receptors) by only 16%. The results suggest that the luminal V1-receptor effect of AVP on JK was mediated by the phospholipase C (PLC)/Ca2+/PKC signaling path and not byadenylate cyclase/cAMP/PKA, therefore probably acting on maxi-potassium channels. (AU)

Processo FAPESP: 99/12866-3 - Estudo molecular e funcional de transportadores de íons em membranas
Beneficiário:Gerhard Malnic
Modalidade de apoio: Auxílio à Pesquisa - Temático