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1
Content available remote

Prostaglandins and interleukin-1beta in the hypothalamic-pituitary-adrenal response to systemic phenylephrine under basal and stress conditions

100%
Gadek-Michalska A., Bugajski A. J., Bugajski J.
Journal of Physiology and Pharmacology
|
2008
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tom 59
|
nr 3
563-575
We investigated the role of interleukin-1ß (IL-1ß) and prostaglandins (PG) in the 1-adrenergic agonist, phenylephrine-induced hypothalamic-pituitary-adrenal axis (HPA) responses under basal and social stress conditions. Male Wistar rats, either control or exposed to crowding stress for 7 days prior to treatment, were used in these experiments. All compounds were injected i.p. Cyclooxygenase COX-1 and COX-2 inhibitors, piroxicam and compound NS-398, IL-1ß and IL-1ß receptor antagonist (IL-1ßRA) were injected 15 min before phenylephrine. Plasma ACTH and serum corticosterone levels were measured 1 h after phenylephrine or IL-1ß injection. Phenylephrine, in respective higher dose administered systemically (0.4 mg/kg i.p.) was almost equally effective as given i.c.v. (30 µg) in stimulating ACTH and corticosterone secretion. Likewise, the extent of the involvement of PG generated by COX-1 and COX-2 in the phenylephrine-induced ACTH and corticosterone secretion was similar after systemic or i.c.v. treatment under both resting and stress conditions. Piroxicam, stronger than compound NS-398, reduced the i.p. phenylephrine-induced ACTH and corticosterone secretion. IL-1ß receptor antagonist (50 µg/kg i.p.) did not significantly affect the inhibitory action of piroxicam on the i.p. phenylephrine-induced ACTH and corticosterone secretion in control rats, but significantly enhanced the inhibition evoked by piroxicam in stressed rats. IL-1ß (2.5 µg/kg i.p.) significantly increased ACTH and corticosterone secretion under basal conditions. Crowding stress for 7 days markedly impaired the IL-1ß-induced ACTH and corticosterone secretion. The mechanism of the stimulatory action of i.p. IL-1ß, which does not cross the blood-brain barrier, may comprise both central and peripheral components of the HPA axis. These results suggest that under basal conditions IL-1ß is not markedly involved in the 1-adrenergic agonist-induced stimulation of the HPA axis activity. During social crowding stress IL-1ß and prostaglandins are significantly involved in this stimulation.
2
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Effect of subdiaphragmatic vagotomy and cholinergic agents in the hypothalamic-pituitary-adrenal axis activity

100%
Bugajski A. J., Zurowski D., Thor P., Gadek-Michalska A.
Journal of Physiology and Pharmacology
|
2007
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tom 58
|
nr 2
In the present study, we examined whether the vagus nerve is involved in mediating the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic muscarinic and nicotinic agonists, carbachol and nicotine. The site of HPA axis muscarinic stimulation was determined using peripheral (i.p.) and intracerebroventricular (i.c.v.) administration of carbachol, atropine sulphate (AtrS) and atropine hydrobromide (AtrBr). The i.p. carbachol-(0.5 mg/kg)-induced corticosterone response was significantly reduced by i.p. pretreatment with AtrBr (0.1 mg/kg), but was not diminished by i.c.v. AtrS (0.1µg). The increase in corticosterone secretion induced by i.c.v. carbachol (2 µg) was totally abolished by i.c.v. pretreatment with AtrS (0.1 µg) but was not altered by i.p. AtrBr. Subdiaphragmatic vagotomy performed 2 weeks earlier substantially decreased the i.p. carbachol (0.2 mg/kg)-induced ACTH response and markedly augmented ACTH and corticosterone response to a higher dose of carbachol (0.5 mg/kg) in comparison with the responses in sham operated rats. Vagotomy abolished the stimulatory effect of i.p. nicotine in a low dose (1 mg/kg) on ACTH and corticosterone secretion; the ACTH response to higher dose (2.5 mg/kg) was considerably reduced, while corticosterone response remained unaffected. These results suggest that carbachol given i.c.v. evokes considerable corticosterone response by stimulation of central cholinergic muscarinic receptors. A major part of the i.p. carbachol-induced corticosterone secretion results from peripheral cholinergic muscarinic receptor stimulation. Subdiaphragmatic vagotomy moderately intensified the carbachol-induced ACTH and corticosterone secretion. Vagotomy significantly reduced the nicotine-induced ACTH secretion, possibly by the involvement of vagal afferents. The nicotine-induced corticosterone secretion is not exclusively regulated by circulating ACTH but by various intra-adrenal regulatory components.
3
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Effect of constitutive- and inducible-cyclooxygenase in the carbachol-induced pituitary-adrenocortical response during social stress

100%
Bugajski J., Gadek-Michalska A., Bugajski A. J.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 3
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 rats acts 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 of 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 µg i.c.v.), a cholinergic receptor antagonist, totally abolished the carbachol (2 µg i.c.v.)-induced ACTH and corticosterone secretion and mecamylamine (20 µg i.c.v.), a selective 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. Pretreatment with indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase inhibitor, significantly diminished the ACTH and corticosterone responses to carbachol (0.2 mg/kg i.p.) in control rats and moderately decreased these responses in stressed rats. Piroxicam (0.2 and 2.0 mg/kg i.p.), a COX-1 inhibitor, considerably impaired the carbachol-induced ACTH and corticosterone responses in control rats and markedly diminished these responses in stressed rats. A selective COX-2 blocker, compound NS-398 (0.2 and 2.0 mg/kg i.p.), substantially decreased the carbachol-induced hormones secretion in control rats but did not markedly alter this secretion in stressed rats. These results indicate that in the carbachol-induced HPA axis activation PGs generated by COX-1 are considerably and to a much greater extent involved than PGs generated by COX-2. Social stress markedly diminishes the mediation of PGs generated by COX-1 but PGs synthesized by COX-2 do not substantially participate in the carbachol-induced HPA response.
4
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Content available

Central histaminergic mechanism in the corticosterone response to clonidine

100%
Bugajski J., Gadek-Michalska A., Borycz J., Bugajski A. J.
Journal of Physiology and Pharmacology
|
1993
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tom 44
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nr 3
5
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Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

100%
Bugajski J., Gadek-Michalska A., Bugajski A. J.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,2
The present study examined the functional selectivity of nicotine for nicotinic acetylcholine receptors in the stimulation of the hypothalamic-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 diminished 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 piroxicam, the nicotine-stimulated ACTH and corticosterone response. These results indicate that systemic nicotine stimulates the HPA axis selectively via nicotinic acetylcholine receptors. Chronic social stress significantly impairs the nicotine stimulated ACTH and corticosterone secretion. Prostaglandins, generated by COX-1- but not by COX-2- isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion in both control and stressed rats.
6
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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
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2001
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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.
7
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Content available

Calcium channel blockers impair the pituitary-adrenocortical responses to central adrenergic receptors stimulation

100%
Borycz J., Bugajski A. J., Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
1993
|
tom 44
|
nr 2
8
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Content available

Effect of compound 48-80 on mast cells and biogenic amine levels in brain structures and on corticosterone secretion

100%
Bugajski A. J., Chlap Z., Bugajski J., Borycz J.
Journal of Physiology and Pharmacology
|
1995
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tom 46
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nr 4
9
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Content available

Effect of compound 48-80 on the thalamic mast cells, serotonin level and corticosterone secretion in rats

100%
Bugajski J., Bugajski A. J., Chlap Z., Borycz J.
Journal of Physiology and Pharmacology
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1994
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tom 45
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nr 4
10
Content available remote

Nitric oxide and prostaglandin systems in the stimulation of hypothalamic-pituitary-adrenal axis by neurotransmitters and neurohormones

100%
Bugajski J., Gadek-Michalska A., Bugajski A. J.
Journal of Physiology and Pharmacology
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2004
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tom 55
|
nr 4
The review presents our results on the regulatory role of prostaglandins (PG) and nitric oxide (NO) in the activation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic, adrenergic and histaminergic systems and by neurohormones: corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) under basal conditions. The synthesis of endogenous PG or NO was inhibited by non-selective and selective cyclooxygenase (COX) antagonists and nitric oxide synthase (NOS) blockers given 15 min before the respective receptor agonist and HPA axis activity was assessed 1 h later by measuring plasma ACTH and serum corticosterone levels. The muscarinic agent - carbachol-induced HPA response was considerably supressed by piroxicam, a predominantly constitutive cyclooxygenase (COX-1) inhibitor and significantly diminished by indomethacin, a non-selective COX blocker, but was unaffected by compound NS-398, an inducible cyclooxygenase (COX-2) antagonist. A non-selective NOS antagonist L-NAME and neuronal NOS blocker L-NNA significantly intensified the carbachol-induced corticosterone secretion. The nicotine-induced increase in ACTH and corticosterone response was significantly supressed by piroxicam, and diminished by indomethacin, but was significantly augmented by L-NAME and L-NNA. The inhibition of PG synthesis by indomethacin totally abolished or reversed the increase of nicotine-induced hormone responses to both NOS blockers. The i.c.v. phenylephrine, an alpha1-adrenergic receptor agonist - evoked HPA response was significantly impaired by piroxicam and compound NS-398 and more potently reduced by L-NAME. The i.c.v. clonidine, an alpha2-adrenergic agonist - elicited HPA response was also considerably decreased by piroxicam, compound NS-398 and L-NAME. By contrast, the stimulatory effect of i.c.v. isoprenaline, a non-selective ß-adrenergic agonist, was not altered by either COX or NOS inhibitors. The i.c.v. histamine- and HTMT, a histamine H1-agonist-induced ACTH and corticosterone response were significantly diminished by piroxicam and indomethacin, respectively. Compound NS-398, did not markedly alter the HPA response to HTMT or amthamine, a histamine H2 receptor agonist. Inhibition of endogenous NO synthesis by a neuronal NOS inhibitor 7-nitroindazole markedly enhanced the histamine-induced hormone secretion, abolished the HTMT-induced response and did not substantially alter the amthamine-evoked ACTH and corticosterone secretion. COX blockers did not significantly affect the CRH-induced HPA response and the inhibition of NO synthesis by L-NNA markedly intensified ACTH response. The vasopressin-stimulated increase in HPA response, was considerably reduced by the inhibition of PG synthesis by both COX antagonists while inhibition of NO synthesis by NOS blockers greatly enhanced this response. The involvement of PG and NO in the neurohormonal regulation of HPA activity depends mainly on greatly complex and tightly regulated mechanisms at the level of second messengers IP3 and adenylyl cyclase systems.
11
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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.
12
Content available remote

The involvement of nitric oxide and prostaglandins in the cholinergic stimulation of hypothalamic-pituitary-adrenal response during crowding stress

100%
Bugajski A. J., Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
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2006
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tom 57
|
nr 3
The aim of the present study was to determine the effect of social crowding stress and significance of nitric oxide (NO) and prostaglandins (PG) generated by constitutive and inducible nitric oxide synthase (NOS) and cyclooxygenase (COX) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic muscarinic receptor agonist carbachol. Inhibitors of neuronal NOS (nNOS) L-NNA, general NOS L-NAME and inducible NOS (iNOS) aminoguanidine, as well as inhibitors of COX-1, piroxicam, and COX-2, compound NS-398 were administered 15 min prior to carbachol to control or crowded rats (24 rats in cage for 7, during 3 and 7 days). In stressed rats L-NAME, L-NNA and aminoguanidine significantly intensified the carbachol-induced ACTH and corticosterone secretion, like in control rats. Piroxicam, markedly decreased the carbachol-induced ACTH and corticosterone response under either basal or stress conditions. Compound NS-398 did not markedly alter the carbachol-induced HPA response in control and stressed rats. Crowding stress (3 days) significantly impaired the i.c.v. prostaglandin E2-induced ACTH response. Corticotropin releasing hormone (CRH) receptor antagonists, alpha-helical CRH [9-14], given i.c.v. did not alter the PGE2-evoked corticosterone response in either control or stressed rats, indicating that hypothalamic CRH is not involved in the PGE2-induced central stimulation of HPA axis. In control rats L-NAME considerably enhanced, while L-arginine, a physiological NOS substrate, abolished the PGE2-induced ACTH and corticosterone response. In stressed rats this NOS blocker significantly increased and L-Arg reduced the stimulatory effect of PGE2 on ACTH and corticosterone secretion. The carbachol-induced corticosterone response was significantly increased by pretreatment with nNOS inhibitor L-NNA and was considerably reduced by indomethacin, a general COX inhibitor. Pretreatment with both antagonists left the carbachol-induced corticosterone level unchanged, suggesting an independent and reciprocal effect of NO and PG in the cholinergic stimulation of pituitary-adrenocortical response. These results indicate that in the stimulatory action of muscarinic agonist, carbachol, NO is an inhibitory transmitter under basal and crowding stress conditions. This psychosocial stress does not functionally affect the NOS/NO systems. Prostaglandins are involved in the cholinergic muscarinic-induced stimulation of HPA response to a significant extent in non-stressed rats. PGE2 may be involved in the carbachol-elicited HPA response under basal and stress conditions. Prostaglandins released in response to muscarinic stimulation did not evoke the hypothalamic CRH mediation. NO significantly impairs and PG stimulates the carbachol-induced HPA response in rats under basal and social stress conditions.
13
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Content available

A single corticosterone pretreatment inhibits the hypothalamic-pituitary-adrenal responses to adrenergic and cholinergic stimulation

100%
Bugajski J., Gadek-Michalska A., Bugajski A. J.
Journal of Physiology and Pharmacology
|
2001
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tom 52
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nr 2
14
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Nitric oxide and prostaglandins in the clenbuterol-induced ACTH and corticosterone secretion

100%
Gadek-Michalska A., Bugajski A. J., Bugajski J.
Journal of Physiology and Pharmacology
|
2008
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tom 59
|
nr 1
The present study was designed to determine the involvement of nitric oxide (NO) and prostaglandins (PG) in the stimulatory action of clenbuterol, a selective ß2-adrenergic receptor agonist on hypothalamic-pituitary-adrenal (HPA) axis under basal and social crowding stress conditions. Clenbuterol given i.c.v. (10 µg) or i.p. (0.2 mg/kg) considerably increased ACTH and corticosterone secretion. A selective ß2-receptor antagonist compound ICI 118551 and non-selective ß-receptor antagonist propranolol given by either route reduced the stimulatory action of clenbuterol. Crowding stress (21 rats in a cage for 7) for 3-7 days significantly reduced the i.c.v. clenbuterol-induced ACTH and corticosterone secretion and i.p. clenbuterol-elicited ACTH secretion. L-NAME, mainly endothelial nitric oxide synthase (NOS) blocker, stronger than L-NNA, a neuronal NOS blocker, reduced the clenbuterol-evoked ACTH and corticosterone secretion in control rats but did not significantly alter this secretion already reduced by crowding stress. Piroxicam, predominantly constitutive cyclooxygenase (COX-1) inhibitor, given i.p. significantly diminished the i.p. clenbuterol-induced ACTH and corticosterone secretion in control rats and tended to reverse the reduction of ACTH secretion by crowding stress. These results indicate that clenbuterol, a selective ß2-adrenoceptor agonist, is much stronger stimulator of the HPA axis than isoprenaline, a non-selective ß-receptor agonist. Social crowding stress reduces to a larger extent the HPA response to ß2-receptor stimulation. Likewise, in the HPA axis stimulation via ß2-adrenoceptors endogenous NO and prostaglandins are significantly involved. Beta2-adrenoceptor is a dominant functional subtype of ß-receptor in the stimulatory and modulatory signals regulating the HPA axis activity under basal and social stress conditions.
15
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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
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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.
16
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Effect of cyclooxygenase inhibitors on the CRH-induced pituitary-adrenocortical activity during crowding stress

100%
Bugajski J., Gadek-Michalska A., Bugajski A. J.
Journal of Physiology and Pharmacology
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2003
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tom 54
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nr 1
The aim of the present study was to determine the effect of social stress and significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) under basal and social crowding stress conditions. The stressed rats were crowded in groups of 24 to a cage for 3 or 7 days, whereas the control animals were haused in groups of 7 to a cage of the same size. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. CRH administration. Inhibitors of COX-1, piroxicam (0.2, 2.0, and 5.0 mg/kg), and COX-2, compound NS-398 (0.2 and 2.0 mg/kg), were administered i.p. 15 min prior to CRH (0.1 µg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 3 and 7 days markedly intensifies the stimulatory action of CRH on ACTH secretion. Neither piroxicam nor NS-398 induce any significant effect on the CRH-elicited ACTH and corticosterone secretion in non-stressed or crowded rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the stimulation of HPA axis by CRH under either basal conditions or during crowding stress. These results also indicate that the stimulatory action of CRH on ACTH secretion is not only completely resistant to desensitization but is sensitized during social crowding stress. The results contrast with a significant involvement of PG in the vasopressin-induced stimulation of HPA response during crowding stress.
17

Prostaglandins inhibit the vasopressin-induced corticosterone response

88%
Olowska A., Gadek-Michalska A., Bugajski A. J., Glod R., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1995
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tom 55
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nr 5
18
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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
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tom 45
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nr 3
19
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Content available

Effect of corticotropin releasing hormone on the pituitary-adrenocortical activity under basal and social stress conditions

88%
Bugajski J., Gadek-Michalska A., Olowska A., Borycz J., Bugajski A. J.
Journal of Physiology and Pharmacology
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1994
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tom 45
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nr 4
20
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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
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tom 50
|
nr 2
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