Naslov
Endothelin-mediated phospholipid signalling in the proximal tubule of rat kidney

Autori
Knotek, Mladen ; Jakšić, Ozren ; Selmani, Robert ; Skorić, Boško ; Banfić, Hrvoje

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
The 2nd. European Kidney Research Forum / Klaus Thurau, Giuseppe Remuzzi - Baveno, 1996

Skup
The Second European Kidney Research Forum

Mjesto i datum
Baveno, Italija, 1996

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
endothelin; endothelin receptors; phospholipid signalling; rat kidney; proximal tubule

Sažetak
Enothelin (ET)-mediated phospholipid signalling was studied in the rat proximal tubule. In freshly isolated proximal tubule cells, ET-1, ET-2 and sarafotoxin S6c (S6c) evoked increase in 1, 2 - diacylglycerol (DAG), inositol (1, 4, 5)-trisphosphate and phospho-choline (PCho), suggesting stimulation of both PtdInsP2 and PtdCho specific phospholipases C (PLC), while ET-3 increased only DAG and PCho presumably via PtdCho specific PLC. Renal cortical slice were also stimulated by above mentioned agonists, followed by isolation of etiher bursh border (BBM) or basal-lateral membranes (BLM) in which mass measurements of inositol lipids and DAG were performed. In BBM, DAG increased in response to ET-1, ET-2 and ET-3, and was followed by protein kinase C translocation to the BBM, while in BLM, DAG formation and translocation of PKC was observed only in response to ET-3, suggesting spatial segregation of signalling systems between two membrane domains of proximal tubule cells. Tyrphostine, perutssis (PTX) or cholera (CTX) did not influence ET-mediated signalling in either of membranes suggesting involvement of PTX and CTX insensitive G-protein mediated stimulation of PLCbeta by ET receptors. Since different endothelin were not equipotent in the stimulation of PLC in BBM and BLM, this was used as tool to examine the presence of different ET receptor subtypes in two cell membrane domains. BQ123, an inhibitor of ET(A) receptors, did not prevent ET-1-mediated signalling in BBM, but ET(A, B) antagonist, bosentan, inhibited ET-3-mediated signalling in BBM. In addition, ET(B) agonist, S6c, stimulated PLC in BBM. Neither BQ123 nor bosentan inhibited ET-3 signalling in BLM. Therefore, these data strongly suggest the presence of ET(B) receptors in BBM and ET(C) receptors in BLM, which are coupled to somewhat different phospholipid signalling systems in proximal tubule cells.

Izvorni jezik
Engleski

POVEZANOST RADA