ANGIOTENSIN-II AND BRADYKININ STIMULATE PHOSPHOINOSITIDE BREAKDOWN IN INTACT RAT-KIDNEY GLOMERULI BUT NOT IN PROXIMAL TUBULES - GLOMERULAR RESPONSE MODULATED BY PHORBOL ESTER

被引：34

作者：

SEKAR, MC ^{[1
]}

YANG, M ^{[1
]}

MEEZAN, E ^{[1
]}

PILLION, DJ ^{[1
]}

机构：

[1] UNIV ALABAMA,METAB RES LAB,BIRMINGHAM,AL 35294

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1990年 / 166卷 / 01期

关键词：

D O I：

10.1016/0006-291X(90)91955-R

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We have investigated the effect of angiotensin II, bradykinin, insulin and insulin-like growth factor I on phosphoinositide turnover in intact rat glomeruli and tubules. Angiotensin II produced a dose-dependent increase in inositol monophosphate formation with an IC50 of 10-7 M, when added to isolated rat glomeruli. Angiotensin II-stimulated inositol phosphates formation was inhibited by the angiotensin receptor antagonist [Sar-Leu8]angiotensin II, indicating that the above response was mediated through activation of an angiotensin receptor in intact glomeruli. Besides angiotensin, in intact glomeruli, only bradykinin stimulated a phosphoinositide response, while in intact proximal tubules, none of the agonists tested produced an activation of the inositol phosphate formation. Angiotensin II- and bradykinin-stimulated inositol phosphate accumulation in intact glomeruli was inhibited by phorbol myristate acetate, an activator of protein kinase C. © 1990.

引用

页码：373 / 379

页数：7

共 27 条

[1] MESANGIAL CELL, GLOMERULAR AND RENAL VASCULAR-RESPONSES TO ENDOTHELIN IN THE RAT-KIDNEY - ELUCIDATION OF SIGNAL TRANSDUCTION PATHWAYS [J].