Thoracic aorta was obtained from Wistar rats and VSMCs were isolated from
aorta tissues and then cultured. In vitro cultured VSMCs were stimulated with Ang II (10â€8 mol/l) followed by various doses of PAMP or ADM (10â€9, 10â€8, or 10â€7 mol/l). Cell proliferation as assessed by 3Hâ€TdR incorporation. Protein kinase C (PKC) activity was measured by counting Î³â€32P radioactivity with liquid scintillation. In a separate cohort, in vitro cultured rat aortic vessels were treated with different doses of Ang II or PAMP (10â€9, 10â€8, or 10â€7 mol/l). Cellular and secreted levels of PAMP, ADM and Ang II were measured using radioimmunoassay in the tissues and intubation mediums, respectively.
Ang II (10â€8 mol/l) treatment significantly increased both 3Hâ€TdR incorporation and PKC activity in VSMCs (by 2.68 and 1.02â€fold, respectively; both P<0.01 vs. the control). However, Ang IIâ€ induced elevation of 3Hâ€TdR incorporation, and PKC activity was significantly inhibited by various doses of ADM and PAMP (all P<0.01 vs. the Ang II group). In rat aortic vascular tissues or intubation media, Ang II treatments stimulated the expression and secretion of PAMP and ADM in a doseâ€ dependent manner, while PAMP treatments had no significant effects on Ang II levels. Conclusion: ADM and PAMP inhibit Ang IIâ€induced VSMCs proliferation. The interaction of Ang II, ADM and PAMP may regulate VSMCs and cardiovascular function.