TY - JOUR 
A1 - Priego, Teresa
AU - Ibáñez de Cáceres, Inmaculada
AU - Martín Velasco, Ana Isabel
AU - Villanúa, María de los Ángeles
AU - López-Calderón, Asunción
T1 - Endotoxin administration increases hypothalamic somatostatin mRNA through nitric oxide release
Y1 - 2005
SN - 01670115
UR - http://hdl.handle.net/11268/5528
AB - Acute inflammation induced by endotoxin (LPS) administration inhibits insulin-like growth factor (IGF-I) and growth hormone (GH) secretion. The aim of this study was to elucidate the role of glucocorticoids and nitric oxide (NO) in the effect of LPS on hypothalamic somatostatin gene expression. Adult male Wistar rats were injected with different doses of LPS (5, 10 and 100 μg/kg). Rats received two i.p. injections of LPS (at 17:30 and 8:30 h the following day) and were killed 4 h after the second injection. LPS administration at the dose of 100 μg/kg increased the hypothalamic somatostatin mRNA content, as well as the serum concentrations of corticosterone. Glucocorticoids do not seem to be involved in LPS-induced increase in hypothalamic somatostatin mRNA since adrenalectomy did not prevent this effect. In order to analyze the possible effect of NO, aminoguanidine, an inducible nitric oxide synthase inhibitor, was injected (100 mg/kg s.c.) simultaneously with LPS injection. Aminoguanidine administration did not modify somatostatin mRNA in saline injected rats, but it prevented LPS-induced increase in hypothalamic somatostatin mRNA. These data suggest that the stimulatory effect of endotoxin on hypothalamic somatostatin gene expression is not mediated by glucocorticoids, but instead by the increase in NO release.
KW - Fisiología humana
KW - Farmacología clínica
KW - Fisiología humana
KW - Farmacología
LA - eng
ER -