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1
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Effect of gamma-aminobutyric acid and muscimol on corticosterone secretion in rats

100%
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.
2
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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
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1993
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tom 44
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nr 2
3
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Catecholaminergic regulation of the hypothalamic-pituitary-adrenocortical activity

67%
Bugajski J., Turon M., Gadek-Michalska A., Borycz J. A.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 1
The significance and site of adrenergic receptors involved in the control of the hypothalamic-pituitary-adrenal axis (HPA) activity was assessed indirectly by estimation of serum corticosterone levels 1 h after drug administration to conscious rats. Adrenergic drugs were given intracerebroventricularly (icv) and intraperito neally (ip), the antagonists 15 min prior to the agonists. Noradrenaline, adrenalin and isoproterenol given by either route increased dosedependently the serum corticosterone levels. The corticosterone response to icv noradrenaline was almost abolished by icv pretreatment with propranolol, a ß-adrenergic antagonist, and yohimbine, an α₂ -receptor blocker, and was also considerably reduced by prazosin, an α₂- adrenergic antagonist. When given ip, these antagonists did not significantly influence the noradrenaline induced corticosterone response, which suggests a suprapituitary site of action of noradrenaline in stimulation of the HPA. The corticosterone response to icv adrenalin was suppressed by prazosin given by either route. The corticosterone response to ip adrenalin was almost abolished by pretreatment with yohimbine, and also significantly diminished by propranolol given by the same route. The increase in corticosterone secretion, induced by isoproterenol given by either route, was abolished by ip injection of propranolol. These results indicate that noradrenaline stimulates the HPA via α and ß-adrenergic receptors, mainly at the suprapituitary level. Adrenalin increases that activity both via central and pituitary a and ß-adrenoceptors. Isoproterenol activates the HPA by stimulation of pituitary ß-receptors.
4
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Influence of nitric oxide synthase inhibitors on the vasopressin-induced pituitary-adrenocortical activity and hypothalamic catecholamine levels

67%
Bugajski J., Gadek-Michalska A., Glod R., Borycz J.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 4
5
Content available remote

Effect of cyclooxygenase inhibitors on the vasopressin induced ACTH and corticosterone response during crowding stress

67%
Bugajski J., Gadek-Michalska A.
Journal of Physiology and Pharmacology
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2003
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tom 54
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nr 2
The aim of the present study was to compare the effect of social stress on the corticotropin releasing hormone (CRH) and arginine vasopressin (AVP)-induced pituitary-adrenocortical activity. Also the 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 AVP under basal and crowding stress conditions was investigated. The control rats were housed 7 in a standard cage and stressed rats were crowded 24 in a cage of the same size during 7 days. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. AVP administration. Indomethacin (2.0 mg/kg i.p.), a non-selective COX inhibitor, piroxicam (0.2, 2.0, and 5.0 mg/kg), a more potent COX-1 than COX-2 inhibitor, and compound NS-398 (0.2 and 2.0 mg/kg) a selective COX-2 inhibitor, were administered i.p. 15 min prior to AVP (5.0 µg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 7 days considerably inhibits the stimulatory action of AVP on ACTH secretion, while it intensifies the CRH-induced ACTH secretion. Indomethacin, piroxicam and NS-398 significantly diminished the AVP-elicited ACTH and corticosterone secretion in non-stressed rats. None of these COX antagonist induced any significant inhibition of the AVP-induced ACTH and corticosterone secretion in stressed rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the HPA stimulation by AVP during crowding stress. These results suggest that social crowding stress desensitizes the PG stimulatory mechanism which considerably mediates the AVP-induced HPA stimulation under basal conditions. The results contrast with a lack of any involvement of PG in the CRH-induced stimulation of HPA response under basal or crowding stress conditions.
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