Abstract:
:Using urethane-anesthetized rats, we examined whether an activation of nuclear factor kappa B is involved in the corticotropin-releasing factor-induced increase in plasma levels of catecholamines. An intracerebroventricularly administered corticotropin-releasing factor (1.5 nmol/animal)-induced increase of plasma catecholamines was dose-dependently reduced by pyrrolidine dithiocarbamate (a nuclear factor kappa B antagonist) (1 and 9 nmol/animal, intracerebroventricularly) and SN50 (a peptide inhibiting nuclear factor kappa B translocation) (9 and 18 nmol/animal, intracerebroventricularly), while SN50M (an inactive control peptide for SN50, 19 nmol/animal, intracerebroventricularly) had no effect on the corticotropin-releasing factor-induced elevation of both catecholamines. Furthermore, the corticotropin-releasing factor-induced responses were also attenuated by rosiglitazone (a peroxisome proliferator-activated receptor-gamma agonist)(50 nmol/animal, intracerebroventricularly). These results suggest the involvement of brain nuclear factor kappa B in the corticotropin-releasing factor-induced central activation of the sympatho-adrenomedullary outflow in rats.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Okada S,Yamaguchi-Shima N,Shimizu T,Arai J,Yorimitsu M,Yokotani Kdoi
10.1016/j.ejphar.2008.01.037subject
Has Abstractpub_date
2008-04-14 00:00:00pages
207-12issue
1eissn
0014-2999issn
1879-0712pii
S0014-2999(08)00111-8journal_volume
584pub_type
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