CONICET | Buscador de Institutos y Recursos Humanos

Rats with induced prehepatic portal hypertension (PH) are a model of porto-systemic hepatic encephalopathy (PSHE). Since very little is known about the neuroendocrine changes that occur in PSHE and considering that prolactin (PRL) plays an important role in the maintenance of homeostasis, in the present study we evaluated plasma PRL levels in adult Wistar male rat with PH and the involvement of ammonia, nitric oxide (NO) and dopamine (DA) in the control of PRL secretion in this model. We determined plasma PRL levels by RIA, DA and dihydroxyphenylacetic acid (DOPAC) content in medial basal hypothalamus (MBH) and anterior pituitary (AP) by HPLC. In addition, NO synthase (NOS) activity and protein expression were evaluated in AP by 14C-Arginine method and Western blot respectively. Also, the AP from normal and PH rats were incubated under different concentrations of ammonia and/or a NOS inhibitor (L-NAME) and PRL secretion was determined. Our results showed that plasma PRL levels were significantly decreased in PH rats (p<0.05). However, we did not observe modifications in DA nor DOPAC content, neither DOPAC/DA ratio in both MBH and AP. The NOS activity (p<0.01) and it protein expression (p<0.001) were increased in AP from PH rats. The ammonia significantly reduced PRL secretion from AP in vitro (p<0.01). The presence of L-NAME abrogated the inhibitory effect of PH plus ammonia on PRL secretion. In conclusion we found that plasma PRL levels were decreased in PH rats, probably due to the high ammonia levels and the increase in NO production in AP, since NO inhibits PRL secretion from AP, it could act regardless of the participation of the dopaminergic system.