Is angiotensin II upregulation of cardiomyocyte adiponectin production nitric oxide/cyclic GMP dependent?
These data suggest a mechanism whereby Ang II upregulates adiponectin in NRVMs via the angiotensin type-2 receptor/nitric oxide/cGMP/ protein kinase G signaling pathway.
CLP decreases the spontaneous activity of the RPV as well as the contractile responses to AT(II) and NKB. The vascular failure is correlated to the severity of sepsis. The reactivity to NE is not altered in this model. Neither NO nor prostaglandins are responsible for the vascular abnormalities observed during CLP.