Effect of Angiotensin III on Akt in Wistar Rat VSMCs

Nova Southeastern University, Davie, Florida, USA

Objective. We investigated whether angiotensin (Ang) III induces Protein kinase B (commonly known as Akt) phosphorylation in rat vascular smooth muscle cells (VSMCs). Background. The molecular mechanisms involved in Ang III biological effects have not been fully investigated. Most studies have shown that Akt mediates Ang II inflammatory effects in VSMCs. VSMC inflammation is a critical action associated with cardiovascular diseases including hypertension. The role of Ang III to induce Akt in VSMCs is unknown and was the focus of these studies. Methods. VSMCs were isolated from the thoracic aorta of adult Wistar rats by the explant technique. VSMCs were grown to confluency and growth arrested cells were treated with 0.1 nM to 1000 nM Ang III for 10 minutes, or with 100 nM Ang III for 1 minute to 30 minutes. The Western blotting technique was used to determine the effects of Ang III on Akt protein phosphorylation. Results. Ang III caused a dose-dependent increase in Akt protein phosphorylation. The effects of the peptide on Akt phosphorylation were maximal between 100 nM and 1000 nM. The peptide’s effects were rapid, occurring within minutes of treatment, and the maximal effects on Akt phosphorylation were observed after 15 minutes of Ang III treatment. Conclusion: These findings provide insight into the molecular nature of Ang III actions and offer a possible molecular mechanism by which Ang III physiological actions occur in VSMCs. Grants. This study was partially funded by a Metabolic & Cardiovascular Research fund established in the College of Pharmacy.