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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Amorim, José B. O. ; Musa-Aziz, Raif ; Mello-Aires, Margarida ; Malnic, Gerhard [4]
Total Authors: 4
Document type: Journal article
Source: Kidney International; v. 66, n. 2, p. 696-704, Aug. 2004.
Field of knowledge: Biological Sciences - Physiology

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 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)

FAPESP's process: 99/12866-3 - Molecular and functional studies of ion transporters in membranes
Grantee:Gerhard Malnic
Support type: Research Projects - Thematic Grants