Norepinephrine Uptake Is Enhanced in Discrete Telencephalic and Diencephalic Areas and Nuclei in Prehepatic Portal Hypertensive Rats

Lemberg, A; Perazzo, Juan Carlos; Romay, Salvador; Eizayaga, Francisco Xavier; Vatta, Marcelo S.; Rodrı́guez-Fermepı́n, Martı́n; Bianciotti, Liliana G.; Monserrat, Alberto J.; Fernández, Belisario E.

doi:10.1016/s0361-9230(97)00331-6

Cited by 7 publications

(7 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increase in E and NE content in these brain regions from PH rats probably suppresses the PRL secretion. The remarkable increase in NE in MBH is consistent with the findings of Lemberg et al [23] and Fernandez et al [24] who observed an enhanced NE uptake in several hypothalamic areas. These catecholamines could probably be responsible in part for the decrease in PRL secretion, and they also contributed to the development and maintenance of PH in this animal model.…”

Section: Discussionsupporting

confidence: 91%

“…The increase in NOS induced NO production that inhibits PRL release from the AP, regardless of the participation of the dopaminergic system. Also, the activation of the adrenergic system participates in the suppression of PRL secretion and confirmed the alterations in uptake and release of NE previously reported in this PH rat model [23,24] .…”

Section: Discussionsupporting

confidence: 89%

“…In general, the endocrine changes associated with chronic hepatic failure were attributed to the liver-induced disorder of metabolism of sexual hormones or to the decrease in liver synthesis of protein hormones [21,22] . However, some evidence supports the hypothesis that central catecholamines may play a significant role in the production and/or maintenance of different alterations that characterize PH [23] . We previously documented alterations in uptake and release of NE and modification in tyrosine hydroxylase activity in several hypothalamic nuclei [23][24][25] .…”

Section: Introductionmentioning

confidence: 93%

“…However, some evidence supports the hypothesis that central catecholamines may play a significant role in the production and/or maintenance of different alterations that characterize PH [23] . We previously documented alterations in uptake and release of NE and modification in tyrosine hydroxylase activity in several hypothalamic nuclei [23][24][25] .…”

Section: Introductionmentioning

confidence: 93%

See 3 more Smart Citations

Role of Ammonia and Nitric Oxide in the Decrease in Plasma Prolactin Levels in Prehepatic Portal Hypertensive Male Rats

Scorticati

Perazzo²,

Rettori

et al. 2006

Neuroimmunomodulation

View full text Add to dashboard Cite

Objectives: Since very little is known about neuroendocrine changes that occur in portal-systemic hepatic encephalopathy, we studied plasma prolactin (PRL) levels and the involvement of hyperammonemia, nitric oxide (NO) and dopaminergic and adrenergic systems in the control of this hormone secretion in a male rat model of prehepatic portal hypertension (PH). Methods: We conducted in vivo studies to determine plasma ammonia and PRL levels. Dopamine (DA), dihydroxyphenylacetic acid (DOPAC), epinephrine and norepinephrine content in medial basal hypothalamus (MBH) and anterior pituitary (AP) were measured. In addition, NO synthase (NOS) activity and protein expression were evaluated in APs. In in vitro studies, the APs from intact rats were incubated with different doses of ammonia and PRL secretion was determined. In ex vivo studies, the APs from normal and PH rats were incubated in the presence of ammonia and/or a NOS inhibitor, N^G-nitro-L-arginine-methyl ester (L-NAME) and PRL secretion was determined. Results: PH rats had a significant increase in plasma ammonia levels (p < 0.001) and a decrease in plasma PRL levels (p < 0.05). Neither DA nor DOPAC content or DOPAC/DA ratios were modified in both MBH and APs; however, we observed a significant increase in norepinephrine content in both MBH and AP (p < 0.001 and p < 0.05, respectively) and a significant increase in epinephrine in APs (p < 0.001). Moreover, PH produced an increase in NOS activity (p < 0.01) and NOS protein expression (p < 0.0001) in APs. The ammonia (100 µM) significantly reduced PRL secretion from APs in vitro (p < 0.05). The presence of L-NAME, an inhibitor of NOS, abrogated the inhibitory effect of ammonia on PRL secretion from APs from control and PH rats. Conclusions: We found that plasma PRL levels were decreased in PH rats probably due to the high ammonia levels. The central noradrenergic system could also mediate this decrease. Also, the increase in NOS activity and/or content in AP induced NO production that directly inhibited PRL secretion from the AP, without the participation of the dopaminergic system.

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 93%

See 2 more Smart Citations

Role of Ammonia and Nitric Oxide in the Decrease in Plasma Prolactin Levels in Prehepatic Portal Hypertensive Male Rats

Scorticati

Perazzo²,

Rettori

et al. 2006

Neuroimmunomodulation

View full text Add to dashboard Cite

show abstract

“…�e found changes in norepinephrine´s metabolism in discrete diencephalic regions in PVL rats [167] . Moreover, ascending along the brain stem, we arrived at the hip�� pocampus where we found changes in capillaries and as�� trocytes [168] .…”

Section: Memorymentioning

confidence: 89%

Hepatic encephalopathy: An approach to its multiple pathophysiological features

Perazzo¹,

Tallis²,

Delfante³

et al. 2012

WJH

View full text Add to dashboard Cite

Hepatic encephalopathy (HE) is a neuropsychiatric complex syndrome, ranging from subtle behavioral abnormalities to deep coma and death. Hepatic encephalopathy emerges as the major complication of acute or chronic liver failure. Multiplicity of factors are involved in its pathophysiology, such as central and neuromuscular neurotransmission disorder, alterations in sleep patterns and cognition, changes in energy metabolism leading to cell injury, an oxidative/nitrosative state and a neuroinflammatory condition. Moreover, in acute HE, a condition of imminent threat of death is present due to a deleterious astrocyte swelling. In chronic HE, changes in calcium signaling, mitochondrial membrane potential and long term potential expression, N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations, and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be observed. The main molecule indicated as responsible for all these changes in HE is ammonia. There is no doubt that ammonia, a neurotoxic molecule, triggers or at least facilitates most of these changes. Ammonia plasma levels are increased two-to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite, glutamine (GLN), lead to hyperammonemic conditions. Removal of hepatic ammonia is a differentiated work that includes the hepatocyte, through the urea cycle, converting ammonia into GLN via glutamine synthetase. Under pathological conditions, such as liver damage or liver blood by-pass, the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly ex-HE is rapidly ex-HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be considered. This editorial will focus on issues where, to the best of our knowledge, more research is needed in order to clarify, at least partially, controversial topics.

show abstract

Prehepatic portal hypertension and mitochondrial dysfunction in brain hippocampus

Perazzo¹,

Arnaiz²,

Fernández³

et al.

Hepatic Encephalopathy and Nitrogen Metabolism

View full text Add to dashboard Cite

Norepinephrine Uptake Is Enhanced in Discrete Telencephalic and Diencephalic Areas and Nuclei in Prehepatic Portal Hypertensive Rats

Cited by 7 publications

References 24 publications

Role of Ammonia and Nitric Oxide in the Decrease in Plasma Prolactin Levels in Prehepatic Portal Hypertensive Male Rats

Role of Ammonia and Nitric Oxide in the Decrease in Plasma Prolactin Levels in Prehepatic Portal Hypertensive Male Rats

Hepatic encephalopathy: An approach to its multiple pathophysiological features

Prehepatic portal hypertension and mitochondrial dysfunction in brain hippocampus

Contact Info

Product

Resources

About