Anti-fibrotic mechanisms of angiotensin AT -receptor stimulation.

The angiotensin AT -receptor is a main receptor of the protective arm of the renin-angiotensin system. Understanding of this unconventional G-protein coupled receptor has significantly advanced during the past decade, largely because of the availability of a selective non-peptide AT -receptor agonist, which allowed the conduct of a multitude of studies in animal disease models. This article reviews such preclinical studies that in their entirety provide strong evidence for an anti-fibrotic effect mediated by activation of the AT -receptor.

Identification of protein phosphatase involvement in the AT receptor-induced activation of endothelial nitric oxide synthase.

The Angiotensin II type 2 receptor (ATR) promotes vasodilation by nitric oxide (NO) release from endothelial cells. However, the mechanisms underlying the ATR-induced stimulation of endothelial NO synthase (eNOS) is still not completely understood. Therefore, we investigated whether in addition to the known ATR-mediated phosphorylation of eNOS at Ser, activation of phosphatases and dephosphorylation of eNOS at Tyr and Thr are also involved.