作者: Danielle M. Trappanese , Sarah Sivilich , Hillevi K. Ets , Farah Kako , Michael V. Autieri
DOI: 10.1152/AJPCELL.00311.2015
关键词:
摘要: Vascular smooth muscle contraction is primarily regulated by phosphorylation of myosin light chain. There are also modulatory pathways that control the final level force development. We tested hypothesis protein kinase C (PKC) and mitogen-activated (MAP) modulate vascular activity via effects on MAP phosphatase-1 (MKP-1). Swine carotid arteries were mounted for isometric recording subjected to histamine stimulation in presence absence inhibitors PKC [bisindolylmaleimide-1 (Bis)], (MEK) (U0126), MKP-1 (sanguinarine) flash frozen measurement kinase, PKC-potentiated phosphatase inhibitor 17 (CPI-17), caldesmon levels. CPI-17 was phosphorylated response inhibited Bis. Caldesmon levels increased decreased MEK inhibition but not affected addition Inhibition significantly p42 p44 kinase. with U0126 both activity. sanguinarine blocked Bis-dependent increase Sanguinarine alone due its MKP-1. phosphorylation, which This suggests has a negative feedback role inhibiting Therefore, catalyzes reversed Thus fine tuning concerted effort PKC,