Angiotensin peptides stimulated prostaglandin release in a dose-dependent manner in C6 glioma cells, with ANG-(1-7) being the most potent.
ANG-(1-7) and ANG II stimulate prostaglandin synthesis in rat C6 glioma cells through distinct receptor subtype interactions, primarily involving subtype 1 receptors.
The heptapeptide angiotensin (ANG)-(1-7) mimics some but not all the central actions of ANG II, suggesting that receptor subtypes may exist. The effects of ANG-(1-7), ANG II, and ANG I on prostaglandin (PG) E2 and prostacyclin (PGI2) synthesis were investigated in neurally derived rat C6 glioma cells. All three ANG peptides stimulated PG release in a dose-dependent manner with the order of potency ANG-(1-7) greater than ANG I greater than ANG II. PGE2 release induced by ANG-(1-7) (10(-7) M) was partially blocked by Sar1,Ile8ANG II (10(-6) M), Sar1,Thr8ANG II (10(-6) M), or the subtype 1 selective antagonist Du Pont 753 (10(-5) M) but not by the subtype 2 selective antagonist CGP 42112A (10(-7)-10(-5) M). PGI2 release was inhibited only by Sar1,Thr8ANG II. ANG II-induced PGE2 release was blocked by Sar1,Thr8ANG II (10(-6) M), Sar1,Ile8ANG II (10(-6) M), or Du Pont 753 (10(-7) M) but not by CGP 42112A (10(-7)-10(-5) M). In contrast, ANG II-induced PGI2 release was blocked by Du Pont 753 (10(-7) M) as well as Sar1,Ile8ANG II (10(-6) M) but not by Sar1,Thr8ANG II or CGP 42112A. Thus ANG II-stimulated PGE2 and PGI2 syntheses in C6 glioma cells are mediated via receptor subtype 1. ANG-(1-7)-induced PGE2 synthesis is also mediated via subtype 1 receptors; however, PGI2 release was blocked by Sar1,Thr8ANG II only.(ABSTRACT TRUNCATED AT 250 WORDS)
Jaiswal et al. (1991) studied C6 glioma cells. Angiotensin peptides (ANG-(1-7), ANG II, ANG I) vs. Receptor antagonists was evaluated on Prostaglandin (PG) E2 and prostacyclin (PGI2) synthesis. Angiotensin peptides stimulated prostaglandin release in a dose-dependent manner in C6 glioma cells, with ANG-(1-7) being the most potent.