[Effects of praeruptorin C on cell hypertrophy, intracellular [Ca2+]i, nitric oxide and signal transduction in isolated hypertrophied rat smooth muscle cells induced by angiotensin II].

AIM To investigate the effects of praeruptorin C (Pra C) on smooth muscle cell (SMC) hypertrophy, intracellular calcium ( [Ca 2+ ]i ), nitric oxide (NO) content and influence on cellular signal transduction in isolated cultured rat smooth muscle cell (SMC). METHODS Hypertrophied smooth muscle cells (HSMCs) were induced by angiotensin II (Ang II), cell area was measured under inverted microscope. Nitric oxide (NO) concentration was measured using Griess method. [Ca 2+ ]i was measured using Fura 2/AM. The responses to [Ca 2+ ]i elevation stimulated by KCl (60 mmol·L -1 or norepinephrine (10 μmmol·L -1 ) were observed by incubation with phorbol 12 myristate 13 acetate (PMA), staurosporine (ST), the agonist and inhibitor of protein kinase C (PKC), and pertussis toxin (PTX), the sensitive toxin of Gi. RESULTS The cell area of SMCs were decreased by 39 01% ( P 0 001) and NO content of SMCs were significantly increased in Pra C + Ang II group. In presence of 60 mmol·L -1 KCl or 10 μmol·L -1 NE, [Ca 2+ ]i of SMCs in Pra C + Ang II group was significantly decreased than that of Ang II group ( P 0 001) and closed to the normal group. Incubation of SMCs with PMA, ST and PTX, [Ca 2+ ]i of SMCs in Ang II group was increased by PMA and decreased by ST and PTX, but that of Pra C + Ang II group was similar to the normal group. CONCLUSION These findings suggest that Pra C can reduce vascular hypertrophy in isolated rat HSMCs, and this is associated with improvment of SMCs [Ca 2+ ]i level, NO content and cellular signal transdution of PKC and Gi.