| dc.contributor | Universidade Estadual Paulista (UNESP) | |
| dc.creator | Amorim, JBO | |
| dc.creator | Musa-Aziz, R. | |
| dc.creator | Mello-Aires, M. | |
| dc.creator | Malnic, G. | |
| dc.date | 2014-05-20T15:27:38Z | |
| dc.date | 2016-10-25T18:02:30Z | |
| dc.date | 2014-05-20T15:27:38Z | |
| dc.date | 2016-10-25T18:02:30Z | |
| dc.date | 2004-08-01 | |
| dc.date.accessioned | 2017-04-06T00:03:06Z | |
| dc.date.available | 2017-04-06T00:03:06Z | |
| dc.identifier | Kidney International. Malden: Blackwell Publishing Inc., v. 66, n. 2, p. 696-704, 2004. | |
| dc.identifier | 0085-2538 | |
| dc.identifier | http://hdl.handle.net/11449/37586 | |
| dc.identifier | http://acervodigital.unesp.br/handle/11449/37586 | |
| dc.identifier | 10.1111/j.1523-1755.2004.00800.x | |
| dc.identifier | WOS:000222578400033 | |
| dc.identifier | WOS000222578400033.pdf | |
| dc.identifier | http://dx.doi.org/10.1111/j.1523-1755.2004.00800.x | |
| dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/880865 | |
| dc.description | Background. Previous studies from our laboratory have shown that luminal perfusion with arginine vasopressin (AVP) stimulates distal tubule secretory potassium flux (J(K)) via V1 receptors (Am J Physiol 278: F809- F816, 2000). In the present work, we investigate the cell signaling mechanism of this process.Methods. In vivo stationary microperfusion was performed in rat cortical distal tubules and luminal K was measured using double K+ resin/reference microelectrodes.Results. In control conditions, J(K) 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 [phorbol 12-myristate 13-acetate (PMA), which activates protein kinase C (PKC)]. During luminal perfusion with 10(-11) mol/L AVP, J(K) increased to 0.88 +/- 0.08 nmol. cm(-2).seconds(-1). In the presence of 10(-11) mol/L AVP, J(K) 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 x 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 J(K) by 36.4%, and AVP-independent J(K) (after blocking V1 receptors) by only 16%.Conclusion. The results suggest that the luminal V1-receptor effect of AVP on J(K) was mediated by the phospholipase C (PLC)/ Ca2+/PKC signaling path and not by adenylate cyclase/cAMP/PKA, therefore probably acting on maxi-potassium channels. | |
| dc.language | eng | |
| dc.publisher | Blackwell Publishing | |
| dc.relation | Kidney International | |
| dc.rights | info:eu-repo/semantics/closedAccess | |
| dc.subject | potassium | |
| dc.subject | distal tubule | |
| dc.subject | PKC | |
| dc.subject | maxi-potassium channels | |
| dc.subject | cell signaling | |
| dc.subject | cAMP | |
| dc.subject | staurosporin | |
| dc.title | Signaling path of the action of AVP on distal K+ secretion | |
| dc.type | Otro | |
