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1
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Role of prostaglandins and nitric oxide in the lipopolysaccharide-induced ACTH and corticosterone response

100%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2004
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tom 55
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nr 3
This study was designed to determine the role of endogenous prostaglandins (PG) and nitric oxide (NO) in the lipopolysaccharide (LPS)-induced ACTH and corticosterone secretion in conscious rats. LPS (0.5 and 1 mg/kg) given i.p. stimulated the hypothalamic-pituitary-adrenocortical (HPA) activity measured 2 h later. A non-selective cyclooxygenase inhibitor indomethacin (10 mg/kg i.p.), piroxicam (2 mg/kg i.p.), a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (2 mg/kg i.p.), a selective inhibitor of inducible cyclooxygenase (COX-2) given 30 min before LPS (1 mg/kg i.p.) significantly diminished both the LPS-induced ACTH and corticosterone secretion. COX-2 blocker was the most potent inhibitor of ACTH secretion (72.3%). Nw-nitro-L-arginine methyl ester (L-NAME 2 and 10 mg/kg i.p.), a non-selective nitric oxide synthase (NOS) blocker given 15 min before LPS did not substantially alter plasma ACTH and corticosterone levels 2 h later. Aminoguanidine (AG 100 mg/kg i.p.), a selective inducible nitric oxide synthase (iNOS) inhibitor, considerably enhanced ACTH and corticosterone secretion induced by a lower dose (0.5 mg/kg) of LPS and did not significantly alter this secretion after a larger dose (1 mg/kg) of LPS. L-NAME did not markedly affect the indomethacin-induced inhibition of ACTH and corticosterone response. By contrast, aminoguanidine abolished the indomethacin-induced reduction of ACTH and corticosterone secretion after LPS. These results indicate an opposite action of PG generated by cyclooxygenase and NO synthesized by iNOS in the LPS-induced HPA-response.
2
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Effect of gamma-aminobutyric acid and muscimol on corticosterone secretion in rats

86%
Borycz J., Borycz J. A., Bugajski J.
Journal of Physiology and Pharmacology
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1992
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tom 43
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nr 3
The effect of γ-aminobutyric acid-receptor agonists, GABA and muscimol on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, and the receptors involved were investigated in conscious rats. GABA given ip induced a dual effect, in lower dose (10mg/kg) it significantly decreased the resting serum corticosterone levels while in higher doses (100-500mg/kg) it considerably raised that level. Muscimol (0.5mg/kg ip) also increased the corticosterone concentration. Both GABA and muscimol given intracerebroventricularly (icv) induced a significant, dose-related increase in serum corticosterone levels. Bicuculline, a GABAA-receptor antagonist, totally abolished the corticosterone response to GABA but did not influence the response to muscimol. Pretreatment with atropine did not affect the corticosterone response to GABA but significantly diminished the response to muscimol. These results suggest that GABA moderately inhibits the pituitary-adrenal axis at the pituitary level but significantly stimulates it at the hypothalamic level. The stimulatory effect of GABA, but not muscimol, is mediated by hypothalamic GABA A-receptors, and in the effect of muscimol hypothalamic cholinergic, muscarinic receptors are involved to a significant extent.
3
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Involvement of constitutive (COX-1) and inducible cyclooxygenase (COX-2) in the adrenergic-induced ACTH and corticosterone secretion

86%
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
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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.
4
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The influence of indomethacin on the ACTH secretion induced by central stimulation of adrenergic receptors

86%
Glod R., Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 2
5
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Effect of adrenergic antagonists and cyclooxygenase inhibitors on the nicotine-induced hypothalamic-pituitary-adrenocortical activity

86%
Gadek-Michalska A., Bugajski J., Bugajski A. J., Glod R.
Journal of Physiology and Pharmacology
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2002
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tom 53
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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.
6
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Repeated handling, restraint, or chronic crowding impair the hypothalamic-pituitary-adrenocortical response to acute restraint stress

86%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
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2003
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tom 54
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nr 3
The purpose of the present study was to assess whether, and to what extent prior handling, restraint or social crowding stress during 3-10 days affects the hypothalamic-pituitary-adrenocortical (HPA) response to an acute short-lasting restraint stress. Also the effect of a feedback inhibitory mechanism of corticosterone in the impairment of HPA axis by these stressors was investigated. Male Wistar rats were pretreated with handling 1 min/day for 3-10 days, restraint 2 times daily for 3-7 days and crowding stress for 7 days before exposure to acute restraint stress in metal tubes for 10 min. Some group of rats received exogenous s.c. corticosterone either once 25mg/kg or 2 times daily 10 mg/kg for 3-10 days before restraint stress. After the last restraint the rats were decapitated and their trunk blood was collected for the measurement of plasma ACTH and serum corticosterone levels. Handling for 3-7 days, restraint for 3-7 days, and crowding for 7 days and a single pretreatment with corticosterone - all significantly and to a similar extent inhibited the restraint stress-induced increase in ACTH and corticosterone secretion. Chronic pretreatment with corticosterone blunted the restraint stress-induced increase in HPA axis activity. These results indicate that repeated short-lasting stress induced by handling, restraint, or crowding potently attenuates the acute restraint stress-induced stimulatory action of the HPA axis. They also indicate adaptive action of moderate stress on the HPA axis response to acute stress. The results also suggest that a short-lasting hypersecretion of corticosterone during psychological stress may induce a prolonged feedback inhibition of the HPA axis activity. The attenuation of HPA axis response by prior handling has also obvious methodological implications.
7
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Nitric oxide and prostaglandins in the clenbuterol-induced ACTH and corticosterone secretion

86%
Gadek-Michalska A., Bugajski A. J., Bugajski J.
Journal of Physiology and Pharmacology
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2008
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tom 59
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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.
8
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Role of nitric oxide in the vasopressin-induced corticosterone secretion in rats

72%
Bugajski J., Gadek-Michalska A., Olowska A., Borycz J., Glod R.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 4
9

Circadian variation of corticosterone in adrenal vein blood in rats exposed to different light conditions

72%
Ostrowska Z., Zwirska-Korczala K., Buntner B., Kos-Kudla B.
Bulletin of the Polish Academy of Sciences. Biological Sciences
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1993
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tom 41
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nr 1
10
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Content available

Effect of L-NAME, a specific nitric oxide synthase inhibitor, on corticotropin-releasing hormone-elicited ACTH and corticosterone secretion

72%
Bugajski J., Borycz J., Gadek-Michalska A., Glod R.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 4
11
Content available remote

Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

72%
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 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.
12
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Content available

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

72%
Bugajski J., Gadek-Michalska A., Glod R., Borycz J., Bugajski A. J.
Journal of Physiology and Pharmacology
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1999
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tom 50
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nr 2
13
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Chronic stress adaptation of the nitric oxide synthases and IL-1beta levels in brain structures and hypothalamic-pituitary-adrenal axis activity induced by homotypic stress

58%
Gadek-Michalska A., Tadeusz J., Rachwalska P., Bugajski J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 3
14
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Content available

Involvement of the central noradrenergic system in cholinergic stimulation of the pituitary-adrenal response

58%
Bugajski J., Borycz J., Gadek-Michalska A.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 2
15
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Content available

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

58%
Bugajski A. J., Koprowska B., Thor P., Glod R., Bugajski J.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 4,2
16
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Content available

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

58%
Bugajski J., Borycz J., Gadek-Michalska A., Glod R., Bugajski A. J.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 2
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