Monomeric adiponectin modulates nitric oxide release and calcium movements in porcine aortic endothelial cells in normal/high glucose conditions.

摘要: Abstract Aims Perivascular adipose tissue can be involved in the process of cardiovascular pathology through release adipokines, namely adiponectins. Monomeric adiponectin has been shown to increase coronary blood flow anesthetized pigs increased nitric oxide (NO) and involvement receptor 1 (AdipoR1). The present study was therefore planned examine effects monomeric on NO Ca2 + transients porcine aortic endothelial cells (PAEs) normal/high glucose conditions related mechanisms. Main methods PAEs were treated with alone or presence intracellular kinases blocker, AdipoR1 Ca2 +-ATPase pump inhibitors. role Na+/Ca2 + exchanger examined experiments performed zero Na+ medium. measured specific probes. Key findings In PAE cultured normal conditions, elevated production [Ca2 +]c. Similar observed high although response lower not transient. mobilized by originated from an pool thapsigargin- ATP-sensitive extracellular space. Moreover, prevented kinase blockers inhibitor. Finally, condition, a for restoring found. Significance Our results add new information about control function elicited adiponectin, which would achieved modulation transients. A signalling Akt, ERK1/2 p38MAPK downstream involved.