scholarly journals Roles of Na+/H+ Exchanger Type 1 and Intracellular pH in Angiotensin II-Induced Reactive Oxygen Species Generation and Podocyte Apoptosis

2013 ◽  
Vol 122 (3) ◽  
pp. 176-183 ◽  
Author(s):  
Ya Liu ◽  
Hirofumi Hitomi ◽  
Suwarni Diah ◽  
Kazushi Deguchi ◽  
Hirohito Mori ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Intracellular Ph ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Reactive Oxygen Species–Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor mRNA by Angiotensin II

Hypertension ◽  
2001 ◽  
Vol 37 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Toshihiro Ichiki ◽  
Kotaro Takeda ◽  
Tomotake Tokunou ◽  
Yuko Funakoshi ◽  
Kiyoko Ito ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Receptor Mrna

scholarly journals COX-1-derived PGE2 and PGE2 type 1 receptors are vital for angiotensin II-induced formation of reactive oxygen species and Ca2+ influx in the subfornical organ

2013 ◽  
Vol 305 (10) ◽  
pp. H1451-H1461 ◽  
Author(s):  
Gang Wang ◽  
Pallabi Sarkar ◽  
Jeffrey R. Peterson ◽  
Josef Anrather ◽  
Joseph P. Pierce ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Subfornical Organ ◽  
Prostaglandin E ◽  
Oxygen Species ◽  
Ang Ii ◽  
Cox 1

Regulation of blood pressure by angiotensin II (ANG II) is a process that involves the reactive oxygen species (ROS) and calcium. We have shown that ANG-II type 1 receptor (AT1R) and prostaglandin E2 (PGE2) type 1 receptors (EP1R) are required in the subfornical organ (SFO) for ROS-mediated hypertension induced by slow-pressor ANG-II infusion. However, the signaling pathway associated with this process remains unclear. We sought to determine mechanisms underlying the ANG II-induced ROS and calcium influx in mouse SFO cells. Ultrastructural studies showed that cyclooxygenase 1 (COX-1) codistributes with AT1R in the SFO, indicating spatial proximity. Functional studies using SFO cells revealed that ANG II potentiated PGE2 release, an effect dependent on AT1R, phospholipase A2 (PLA2) and COX-1. Furthermore, both ANG II and PGE2 increased ROS formation. While the increase in ROS initiated by ANG II, but not PGE2, required the activation of the AT1R/PLA2/COX-1 pathway, both ANG II and PGE2 were dependent on EP1R and Nox2 as downstream effectors. Finally, ANG II potentiated voltage-gated L-type Ca2+ currents in SFO neurons via the same signaling pathway required for PGE2 production. Blockade of EP1R and Nox2-derived ROS inhibited ANG II and PGE2-mediated Ca2+ currents. We propose a mechanism whereby ANG II increases COX-1-derived PGE2 through the AT1R/PLA2 pathway, which promotes ROS production by EP1R/Nox2 signaling in the SFO. ANG II-induced ROS are coupled with Ca2+ influx in SFO neurons, which may influence SFO-mediated sympathoexcitation. Our findings provide the first evidence of a spatial and functional framework that underlies ANG-II signaling in the SFO and reveal novel targets for antihypertensive therapies.

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