Role of ghrelin on nitric oxide synthesis and vasopressin during endotoxemic shock

Abstract

The currently prevailing hypothesis is that part of the clinical manifestations that occur during sepsis is caused by an excessive response of the host against infection, an inflammatory response leading to uncontrolled. Several features of sepsis can be reproduced experimentally by administration of lipopolysaccharide (LPS), a component of the external wall of Gram-negative bacteria. During septic shock, multiple hormonal control systems are strongly stimulated at the onset of clinical and subsequently undergo a process of decline. This is especially true with catecholamines and vasopressin (AVP), which contributes to the refractory hypotension characteristic of this clinical state. Another factor that has been considered part of refractory hypotension in septic shock is nitric oxide (NO). This endogenous gaseous modulator, which is synthesized in large quantities during the inflammatory process, also has important vasodilator action, and participates as a modulator of hormone release, among which the AVP. Ghrelin mouse is a peptide of 28 amino acids, where the three serine residues is essential for its function. It is found predominantly in the stomach, but for this peptide immunoreactive neurons were also found in hypothalamic nuclei. Recent studies show that ghrelin has antiapoptotic actions through the activation of PI3K-Akt pathway in cardiomyocytes, endothelial cells, pancreatic cells and neurons. Still, in a study conducted in humans, there was the action of ghrelin on the activation of the hypothalamic-pituitary axis. But there is no data in the literature assessing the involvement of ghrelin on plasma concentrations of AVP and NO during septic shock. Thus, our study is to assess the involvement of ghrelin on plasma concentrations of AVP and NO and its cardiovascular effects in animals subjected to shock endotoxêmico induced by LPS administration. (AU)