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Novara di Sicilia, Italy

Grossini E.,University Eastern Piedmont ogadro | Prodam F.,Azienda Ospedaliera Universitaria Maggiore della Carita | Prodam F.,Health Science University | Walker G.E.,Azienda Ospedaliera Universitaria Maggiore della Carita | And 10 more authors.
Journal of Endocrinology | Year: 2014

Adiponectin, the most abundant adipokine released by adipose tissue, appears to play an important role in the regulation of vascular endothelial and cardiac function. To date, however, the physiological effects of human monomeric adiponectin on the coronary vasculature andmyocardial systo-diastolic function, as well asonparasympathetic/sympathetic involvement and nitric oxide (NO) release, have not yet been investigated. Thus, weplanned to determine the primary in vivo effects of human monomeric adiponectin on coronary blood flow and cardiac contractility/relaxation and the related role of autonomic nervous system, adiponectin receptors, and NO. In 30 anesthetized pigs, human monomeric adiponectin was infused into the left anterior descending coronary artery at constant heart rate and arterial bloodpressure, and the effectsoncoronary bloodflow, left ventricular systo-diastolic function, myocardial oxygen metabolism, and NO release were examined. The mechanisms of the observedhemodynamic responses were also analyzed by repeating the highest dose of human monomeric adiponectin infusion after autonomic nervous systemand NO blockade, and after specific adiponectin 1 receptor antagonist administration. Intracoronary human monomeric adiponectin caused dose-related increases of coronary blood flowand cardiac function. Those effects were accompanied by increased coronary NO release and coronary adiponectin levels. Moreover, the vascular effects of the peptide were prevented by blockade of β2-adrenoceptors and NO synthase, whereas all effects of human monomeric adiponectin were prevented by adiponectin 1 receptor inhibitor. In conclusion, human monomeric adiponectin primarily increased coronary blood flow and cardiac systo-diastolic function through the involvement of specific receptors, β2-adrenoceptors, and NO release. © 2014 Society for Endocrinology. Source


Grossini E.,University Eastern Piedmont ogadro | Gramaglia C.,University Eastern Piedmont ogadro | Farruggio S.,University Eastern Piedmont ogadro | Bellofatto K.,University Eastern Piedmont ogadro | And 4 more authors.
Vascular Pharmacology | Year: 2014

Changes in endothelial function and peroxidation could play a significant role in the pathophysiology of cardiovascular disease in psychiatric patients. In particular, endothelial nitric oxide (NO) could either exert a beneficial or detrimental effect depending on the involvement of NO synthase (NOS) subtype. Therefore, we planned to examine the effects of asenapine on NO release and protection against oxidative stress in porcine coronary endothelial cells (CEC). The Griess system and Western blot were used for NO detection and to examine changes in protein activation and expression. In addition, cell oxidative/antioxidant status and mitochondrial membrane potential were measured by specific fluorescent dyes. Asenapine caused a concentration-dependent increase of NO production (p<0.05) by the involvement of cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA), phospholipase C (PLC), β2-adrenoceptor-related pathway, Akt, extracellular-signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen-activated protein kinases (p38 MAPK). Furthermore, asenapine protected CEC against oxidative stress by preventing reactive oxygen species production and glutathione reduction, mitochondrial membrane potential collapse and apoptosis, and by modulation of the inducible NOS (iNOS). In conclusion, in CEC asenapine induced eNOS-dependent NO production through an intracellular signaling leading to Akt, ERK1/2 and p38MAPK activation. Moreover, asenapine protected CEC against oxidative stress by modulation of antioxidant system, apoptosis, cell survival signaling and mitochondria functioning. © 2014 Elsevier Inc. Source

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