Smooth muscle-selective CPI-17 expression increases vascular smooth muscle contraction and blood pressure

摘要: Recent data revealed that protein kinase C-potentiated myosin phosphatase inhibitor of 17 kDa (CPI-17), a inhibitory preferentially expressed in smooth muscle, is upregulated/activated several diseases but whether this CPI-17 increase plays causal role pathologically enhanced vascular muscle contractility and blood pressure remains unclear. To address possibility, we generated muscle-specific transgenic mouse model (CPI-17-Tg) demonstrated the transgene was selectively muscle-enriched tissues, including mesenteric arteries. The isometric contractions isolated second-order branch artery helical strips from CPI-17-Tg mice were significantly compared with controls response to phenylephrine, U-46619, serotonin, ANG II, high potassium, calcium. perfusion increases perfused beds norepinephrine also mice. hypercontractility associated increased phosphorylation 20-kDa light chain under basal stimulated conditions. Surprisingly, levels rho 2 Cα/δ Radiotelemetry measurements However, no remodeling detected by morphometric analysis. Taken together, our results demonstrate expression promotes pressure, implicating pathological significant upregulation.