Central and peripheral effects of ghrelin over the hypotension induced by endotoxemic shock

Excerpt

Since its discovery by Kojima and colleagues in 1999 [1], the hormone ghrelin has been studied in different contexts, since this peptide has the ability to promote hormonal, vascular and immune changes. His well-established functions are the release of growth hormone, by a mechanism distinct from the growth hormone release factor, and stimulation of hunger, by activating hippothalamic neurons, leading to release of neuropeptide Y, thus promoting orexigenic effects [2]. Because of its ability to release hormones, including vasopressin [3], and by possessing immunomodulatory properties, ghrelin has been studied in different contexts of inflammatory states, as present in endotoxemia and sepsis [4]. The infusion of lipopolysaccharide (LPS) is capable of generating an inflammatory state, with augmenting of TNFα, IL-1β and nitric oxide, which in turn leads to cardiac depression and systemic vasodilation and hypotension [5]. Due to its properties to modulate the inflammatory response, in a way of diminishing the levels of TNFα, IL-1β and nitric oxide, which are augmented in the endotoxemic state, as well the ability to augment the plasma levels of vasopressin, ghrelin emerges as a potential neuro-immunomodulator in hypotension caused by endotoxemia. We speculate that ghrelin, mediating the inflammatory response and by augmenting vasopressin blood levels, could attenuate the hypotension caused by endotoxin. …