Role of Complement 3a in the Synthetic Phenotype and Angiotensin II-Production in Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats

摘要

BackgroundSpontaneously hypertensive rats (SHR)-derived vascular smooth muscle cells (VSMCs) show exaggerated growth with a synthetic phenotype and angiotensin II (Ang II)-production. To evaluate the contribution of complement 3 (C3) or C3a toward these abnormalities in SHR, we examined effects of a C3a receptor inhibitor on proliferation, phenotype, and Ang II-production in VSMCs from SHR and Wistar–Kyoto (WKY) rats.