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1

The significance of central adrenergic system in the met-enkephalin-induced corticosterone secretion

100%
Glod R., Gadek-Michalska A., Olowska A., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
2
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Content available

Influence of nitric oxide synthase inhibitors on the vasopressin-induced pituitary-adrenocortical activity and hypothalamic catecholamine levels

100%
Bugajski J., Gadek-Michalska A., Glod R., Borycz J.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 4
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Effect of L-NAME, a specific nitric oxide synthase inhibitor, on corticotropin-releasing hormone-elicited ACTH and corticosterone secretion

100%
Bugajski J., Borycz J., Gadek-Michalska A., Glod R.
Journal of Physiology and Pharmacology
|
1998
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tom 49
|
nr 4
4
Content available remote

Involvement of constitutive (COX-1) and inducible cyclooxygenase (COX-2) in the adrenergic-induced ACTH and corticosterone secretion

100%
Bugajski J., Glod R., Gadek-Michalska A., Bugajski A. J.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 4,2
The involvement of prostaglandins synthesized by constitutive (COX-1) and inducible cyclooxygenase (COX-2) in central stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists was investigated in conscious rats. COX-1 and COX-2 inhibitor, piroxicam (0.02 and 0.2 µg) and compound NS-398 (0.01 and 0.1 µg), respectively, were given intracerebroventricularly (i.c.v.) 15 min prior to i.c.v. adrenergic receptor agonists: phenylephrine (30 µg) and clonidine (10 µg), an alpha1- and alpha2-adrenergic agonist, and isoprenaline (20 µg) a non-selective ß-adrenergic agonist and clenbuterol (10 µg) a selective ß2-adrenergic agonist. Piroxicam and NS-398 considerably and dose-dependently reduced the phenylephrine-induced increase in ACTH and corticosterone secretion. Pretreatment with piroxicam and NS-398 markedly impaired the clonidine-evoked ACTH and corticosterone secretion. Piroxicam moderately diminished the isoprenaline-elicited increase in ACTH and corticosterone, while NS-398 did not markedly alter ACTH secretion. The clenbuterol-induced ACTH and corticosterone responses were considerably impaired by pretreatment with piroxicam, and slightly less potently by NS-398. These results indicate that in central structures involved in regulation of the HPA axis both constitutive and inducible cyclooxygenase are present under normal conditions in rats. These isoenzymes are significantly involved in the stimulatory signaling transduced by postsynaptic aalpha1-adrenergic receptors and, to a lesser extent, by a2-adrenergic receptors. Both isoenzymes affect moderately the stimulatory action of a non-selective ß-adrenergic agonist on ACTH and corticosterone secretion. COX-1 participates considerably and COX-2 markedly in the potent stimulatory action of selective ß2-adrenergic receptors on HPA axis.
5
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Effect of indomethacin on nicotine-induced ACTH and corticosterone response

100%
Bugajski J., Gadek-Michalska A., Borycz J., Glod R.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 1
6
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The influence of indomethacin on the ACTH secretion induced by central stimulation of adrenergic receptors

100%
Glod R., Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 2
7
Content available remote

Effect of adrenergic antagonists and cyclooxygenase inhibitors on the nicotine-induced hypothalamic-pituitary-adrenocortical activity

100%
Gadek-Michalska A., Bugajski J., Bugajski A. J., Glod R.
Journal of Physiology and Pharmacology
|
2002
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tom 53
|
nr 2
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 system and prostaglandins 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 alpha1-adrenergic antagonist, significantly decreased the nicotine-evoked ACTH and corticosterone secretion. Yohimbine (0.1-1.0 mg/kg), an alpha2-adrenergic antagonist, moderately diminished ACTH response, and propranolol (0.1-10 mg/kg), a ß-adrenergic antagonist, did not significantly alter the nicotine-induced hormones secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably impaired the nicotine-induced ACTH and corticosterone secretion. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker did not markedly alter these hormones secretion, and indomethacin (2 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 and prostaglandins are significantly involved in this stimulation. Noradrenaline, stimulating postsynaptic aplha1-adrenergic receptors, and prostaglandins, synthesized by COX-1 isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion.
8
Content available remote

Effect of social stress on COX-1 and COX-2-induced alterations in the adrenergic agonists-evoked hypothalamic-pituitary-adrenal responses

100%
Bugajski J., Gadek-Michalska A., Glod R., Bugajski A. J.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 4,2
The purpose of the present study was to investigate the contribution of prostaglandins (PGs) synthesized by constitutive (COX-1) and inducible (COX-2) cyclooxygenase to stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists in rats under social crowing stress 3 days, (21 per a cage for 6) animals. The effects of phenylephrine, clonidine and isoprenaline, an alpha1-, alpha2- and ß-adrenergic agonist, respectively, in the presence and absence of COX-1 inhibitor, piroxicam, and COX-2 inhibitor, compound NS-398, on ACTH and corticosterone secretion in stressed rats were compared with these effects in non-stressed animals. All drugs were given intracerebroventricularly (i.c.v.), COX inhibitors 15 min before adrenergic agonists. Piroxicam (0.02 µg) and NS-398 (0.1 µg) significantly reduced the phenylephrine (30 µg) -induced ACTH and corticosterone secretion in both stressed and non-stressed rats. Piroxicam (0.02 µg) and NS-398 (0.01 µg) moderately decreased the clonidine (10 µg) -evoked hormone responses in control rats but did not alter these responses in stressed rats. Piroxicam (0.2 µg) and NS-398 (0.1µg) moderately diminished the isoprenaline (20 µg)-evoked ACTH and corticosterone response in control rats, while in stressed rats these inhibitors did not significantly alter the isoprenaline-induced rise in ACTH and corticosterone secretion. These results indicate that in hypothalamic structures involved in the regulation of adrenergic agonists-induced HPA stimulation COX-2 is expressed under physiological synaptic activity. Social crowding stress does not alter the significant involvement of prostaglandins in the HPA response induced by stimulation of central alpha1-adrenergic receptors. Prostaglandins are of lesser importance in activation of the HPA axis by alpha2-and ß-adrenergic receptors under basal and social stress conditions.
9

The involvement of central adrenergic mechanism in the pituitary-adrenocortical response to cholinergic stimulation

88%
Borycz J., Gadek-Michalska A., Glod R., Olowska A., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
10

Involvement of histamine in the CRH and vasopressin-induced pituitary-adrenocortical response

88%
Olowska A., Gadek-Michalska A., Borycz J., Glod R., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
11

Prostaglandins inhibit the vasopressin-induced corticosterone response

88%
Olowska A., Gadek-Michalska A., Bugajski A. J., Glod R., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
12

Prostaglandins mediate the pituitary-adrenocortical stiulation by adrenergic agonists

88%
Gadek-Michalska A., Borycz J., Olowska A., Glod R., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
13
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Role of nitric oxide in the vasopressin-induced corticosterone secretion in rats

88%
Bugajski J., Gadek-Michalska A., Olowska A., Borycz J., Glod R.
Journal of Physiology and Pharmacology
|
1997
|
tom 48
|
nr 4
14
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Central histaminergic mechanisms madiate the vasopressin-induced pituitary adrenocortical stimulation

88%
Bugajski J., Gadek-Michalska A., Olowska A., Borycz J., Glod R.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 4
15
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

The role of prostaglandins and the hypothalamic and hippocampal histamine in the clonidine-induced pituitary-adrenocortical response

88%
Bugajski J., Gadek-Michalska A., Borycz J., Glod R., Olowska A.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 3
16
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Histaminergic components in carbachol -induced pituitary-adrenocortical activity

88%
Bugajski J., Gadek-Michalska A., Borycz J., Bugajski A. J., Glod R.
Journal of Physiology and Pharmacology
|
1994
|
tom 45
|
nr 3
17
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Blockade of nitric oxide formation impairs adrenergic-induced ACTH and corticosterone secretion

88%
Bugajski J., Gadek-Michalska A., Glod R., Borycz J., Bugajski A. J.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 2
18
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Involvement of nitric oxide in central histaminergic stimulation of the hypothalamic-pituitary-adrenal axis

88%
Bugajski A. J., Koprowska B., Thor P., Glod R., Bugajski J.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 4,2
19
Content available remote

Influence of cyclooxygenase inhibitors on the central histaminergic stimulation of hypothalamic-pituitary-adrenal axis

88%
Bugajski A. J., Thor P., Glod R., Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 4
Brain histamine participates in central regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Endogenous prostaglandins modulate signal transduction of different neurotransmitters involved in activation of HPA axis. In the present experiment we investigated whether endogenous prostaglandins are involved in the stimulation of ACTH and corticosterone secretion by histaminergic systems in the rat brain. Histamine (50 µg), histamine-trifluoromethyl-toluidine derivative (HTMT, 75 µg) a selective and potent H1-receptor agonist, and amthamine (50 µg) a H2-receptor agonist given intracerebroventricularly (i.c.v.) to non-anesthetized rats considerably increased ACTH and corticosterone secretion 1h after administration. A non-selective cyclooxygenase inhibitor indomethacin (2 mg/kg i.p. or 10 µg i.c.v.), piroxicam (0.02 and 0.2 µg i.c.v.) a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (0.1 and 1.0 µg i.c.v.), a selective inhibitor of inducible cyclooxygenase (COX-2) were given 15 min before histamine and histamine receptor agonists. One hour after the last injection trunk blood from decapitated rats was collected for hormones determination. The histamine-induced ACTH and corticosterone secretion was significantly diminished by piroxicam and was not markedly altered by indomethacin and compound NS-398. The HTMT-elicited increase in ACTH and corticosterone secretion was significantly prevented by indomethacin and was not affected by piroxicam or compound NS-398. The amthamine-evoked increase in ACTH and corticosterone secretion was not markedly influenced by any cyclooxygenase blocker applied in the present experiment. These results indicate that the histamine H1-receptor transmitted central stimulation of the HPA axis is considerably mediated by prostaglandins generated by consititutive cyclooxygenase, whereas stimulation transmitted via H2-receptor does not significantly depend on endogenous prostaglandins mediation.
20
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Mediation by nitric oxide of the carbachol-induced corticosterone secretion in rats

88%
Bugajski J., Borycz J., Gadek-Michalska A., Glod R., Bugajski A. J.
Journal of Physiology and Pharmacology
|
1997
|
tom 48
|
nr 2
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