Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: GĄDEK-MICHALSKA
Liczba odnalezionych rekordów: 3



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Tytuł oryginału: Effect of adrenergic antagonists and cyclooxygenase inhibitors on the nicotine-induced hypothalamic-pituitary-adrenocortical activity.
Autorzy: Gądek-Michalska A[nna], Bugajski J., Bugajski A.J., Głód R.
Źródło: J. Physiol. Pharmacol. 2002: 53 (2) s.275-287, il., bibliogr. 24 poz.
Sygnatura GBL: 302,092

Hasła klasyfikacyjne GBL:
  • endokrynologia
  • farmacja

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Nicotine is a potent stimulus for the hypothalamic-pituitary-adrenal (HPA) axis. Systemic nicotine acts via central mechanisms to stimulate by multiple pathways the release of ACTH from the anterior pituitary corticotrops and corticosterone from the adrenal cortex. Nicotine may stimulate indirectly the hypothalamic paraventricular nucleus, the site of the corticotropin-releasing hormone (CRH) neurons which activates ACTH release. In the present studies an involvement of adrenergic systeman dprostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats was investigated. Nicotine (2.5-5 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 hr after administration. Adrenergic receptor antagonists or COX inhibitors were injected i.p. 15 min prior to nicotine and the rats were decapitated 1 hr after the last injection. Prazosin (0.01-0.1 mg/kg), an ŕ1-adrenergic antagonist, significantly decreased th enicotine-evoked ACTH and corticosterone secretion. Yohimbine (0.1 - 1.0 mg/kg), an ŕ2-adrenergic antagonist, moderately diminished ACTH response, and propranolol (0.1 - 10 mg/kg), a á-adrenergic antagonist, did not significantly after the nicotin-induced hormones secretion. Pretreatment with piroxicam (o.2-2.0 mg/kg), a non-selective COX inhibitor significantly diminished ACTH response. These results indicate that systemic nicotine stimulates the HPA axis indirectly, and both adrenergic system ...

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    Tytuł oryginału: Effect of constitutive- and inducible-cyclooxygenase in the carbachol-induced pituitary-adrenocortical response during social stress.
    Autorzy: Bugajski J., Gądek-Michalska A., Bugajski A. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (3) s.453-462, il., bibliogr. 24 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • psychiatria i psychologia
  • endokrynologia

    Typ dokumentu:
  • tytuł obcojęzyczny
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Acetylcholine potently stimulates the hypothalamic-pituitary-adrenal (HPA) axis. Cholinergic receptor agonist carbachol, given intraperitoneally (i.p.) or into the lateral cerebral ventricle (i.c.v.) to non-anesthetized racts via multiple pathways to stimulate the HPA axis. The present study sought to determine 1) the functional selectivity of carbachol for cholinergic muscarinic and/or nicotinic receptors involved in the stimulation of HPA axis; 2) the involvement to prostaglandins (PGs) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the carbachol-induced ACTH and corticosterone secretion in non-stressed rats and animals exposed to social crowding stress for 7 days (24 per a cage for 6). Carbachol was given i.c.v. or i.p and cholinergic receptor antagonists or cyclooxygenase isoenzyme antagonists were given by the same routes 15 min earlier. One hour after the last injection trunk blood was taken for ACTH and corticosterone determinations. Atropine (0.1 ćg i.c.v.), a cholinergic receptor antagonist , totally abolished the carbachol (2 ćg i.c.v.) - induced ACTH and corticosterone secretion and mecamylamine (20 ćg i.c.v.), a selectiove nicotinic receptor antagonist, did not affect this secretion. This finding indicates that carbachol functions as a selective central cholinergic muscarinic receptor agonist for the HPA axis stimulation. Crowding stress significantly diminished the carbachol (0.2 mg/kg i.p.)-induced plasma ACTH and corticosterone levels measured 1 hr after administration. ...

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    Tytuł oryginału: Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress.
    Autorzy: Bugajski J., Gądek-Michalska A., Bugajski A. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 2) s.847-857, il., bibliogr. 31 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • psychiatria i psychologia
  • endokrynologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: The present study examined the functional selectivity of nicotine for nicotinic acetylcholine receptors in the stimulation of the hypothallamic-pituitary-adrenal (HPA) axis, the effect of social crowding stress on HPA response to nicotine and the involvement of prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats crowded (24 per a box instead 7) for 7 days. Nicotine (2.5-5.0 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 h after administration. Mecamylamine (50 mg i.c.v.), a selective nicotinic receptor antagonist, atropine (0.1 mg/kg i.p.) a non-selective cholinergic receptor antagonist, or COX inhibitors were injected 15 min prior to nicotine and the rats were decapitated 1 h after the last injection. Mecamylamine abolished the nicotine-induced ACTH response and significantly deminished corticosterone response. Atropine did not alter ACTH response and modestly diminished corticosterone response to nicotine. Crowding stress significantly impaired the nicotine-evoked ACTH and corticosterone secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably diminished the nicotine-induced ACTH and corticosterone secretion in control and crowded rats. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker, did not markedly alter the nicotine-induced hormones secretion in either control or stressed rats. Indomethacin (2 mg/kg), a non-selective COX inhibitor diminished significantly, but to a lesser extent than...

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