Both subtype 1 and 2 receptors of angiotensin II participate in regulation of intracellular calcium in glomerular epithelial cells

2001 ◽  
Vol 138 (1) ◽  
pp. 40-49 ◽  
Author(s):  
Ram Sharma ◽  
Mukut Sharma ◽  
Susanne Vamos ◽  
Virginia J. Savin ◽  
Thomas B. Wiegmann
1998 ◽  
Vol 274 (3) ◽  
pp. F623-F627 ◽  
Author(s):  
Mukut Sharma ◽  
Ram Sharma ◽  
Andrew. S. Greene ◽  
Ellen T. McCarthy ◽  
Virginia J. Savin

Angiotensin II decreases glomerular filtration rate, renal plasma flow, and glomerular capillary hydraulic conductivity. Although angiotensin II receptors have been demonstrated in mesangial cells and proximal tubule cells, the presence of angiotensin II receptors in glomerular epithelial cells has not previously been shown. Previously, we have reported that angiotensin II caused an accumulation of cAMP and a reorganization of the actin cytoskeleton in cultured glomerular epithelial cells. Current studies were conducted to verify the presence of angiotensin II receptors by immunological and non-peptide receptor ligand binding techniques and to ascertain the activation of intracellular signal transduction in glomerular epithelial cells in response to angiotensin II. Confluent monolayer cultures of glomerular epithelial cells were incubated with angiotensin II, with or without losartan and/or PD-123,319 in the medium. Membrane vesicle preparations were obtained by homogenization of washed cells followed by centrifugation. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of membrane proteins followed by multiscreen immunoblotting was used to determine the presence of angiotensin II receptor type 1 (AT1) or type 2 (AT2). Angiotensin II-mediated signal transduction in glomerular epithelial cells was studied by measuring the levels of cAMP, using radioimmunoassay. Results obtained in these experiments showed the presence of both AT1 and AT2 receptor types in glomerular epithelial cells. Angiotensin II was found to cause an accumulation of cAMP in glomerular epithelial cells, which could be prevented only by simultaneous use of losartan and PD-123,319, antagonists for AT1 and AT2, respectively. The presence of both AT1 and AT2 receptors and an increase in cAMP indicate that glomerular epithelial cells respond to angiotensin II in a manner distinct from that of mesangial cells or proximal tubular epithelial cells. Our results suggest that glomerular epithelial cells participate in angiotensin II-mediated control of the glomerular filtration barrier.


1997 ◽  
Vol 51 (1) ◽  
pp. 301-309 ◽  
Author(s):  
Tamaki Sasaki ◽  
Yoshiyuki Jyo ◽  
Nobuya Tanda ◽  
Yasuhiko Kawakami ◽  
Tsutomu Nohno ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Serina Yokoyama ◽  
Tatsuo Kawai ◽  
Koichi Yamamoto ◽  
Huang Yibin ◽  
Hiroko Yamamoto ◽  
...  

AbstractThe receptor for advanced glycation end-products (RAGE) and the G protein-coupled angiotensin II (AngII) type I receptor (AT1) play a central role in cardiovascular diseases. It was recently reported that RAGE modifies AngII-mediated AT1 activation via the membrane oligomeric complex of the two receptors. In this study, we investigated the presence of the different directional crosstalk in this phenomenon, that is, the RAGE/AT1 complex plays a role in the signal transduction pathway of RAGE ligands. We generated Chinese hamster ovary (CHO) cells stably expressing RAGE and AT1, mutated AT1, or AT2 receptor. The activation of two types of G protein α-subunit, Gq and Gi, was estimated through the accumulation of inositol monophosphate and the inhibition of forskolin-induced cAMP production, respectively. Rat kidney epithelial cells were used to assess RAGE ligand-induced cellular responses. We determined that RAGE ligands activated Gi, but not Gq, only in cells expressing RAGE and wildtype AT1. The activation was inhibited by an AT1 blocker (ARB) as well as a RAGE inhibitor. ARBs inhibited RAGE ligand-induced ERK phosphorylation, NF-κB activation, and epithelial–mesenchymal transition of rat renal epithelial cells. Our findings suggest that the activation of AT1 plays a central role in RAGE-mediated cellular responses and elucidate the role of a novel molecular mechanism in the development of cardiovascular diseases.


1979 ◽  
Vol 15 (1) ◽  
pp. 80-87 ◽  
Author(s):  
Peter M. Andrews ◽  
Marguerite Stauver

Pancreas ◽  
2002 ◽  
Vol 25 (3) ◽  
pp. 290-295 ◽  
Author(s):  
Aaron S. Fink ◽  
Yuanhong Wang ◽  
Tatiana Mendez ◽  
Roger T. Worrell ◽  
Douglas Eaton ◽  
...  

1997 ◽  
Vol 272 (3) ◽  
pp. 1920-1928 ◽  
Author(s):  
Lee M. Graves ◽  
Yaqin He ◽  
John Lambert ◽  
Deborah Hunter ◽  
Xiong Li ◽  
...  

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