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1
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Content available

O działaniu podskórnie wstrzykiwanej adrenaliny na ciśnienie i tętno

100%
Bugajski J.
Acta Physiologica Polonica
|
1955
|
tom 06
|
nr 3
2
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Content available

Wpływ wysiłku fizycznego na ciśnienie i tętno u psów

100%
Bugajski J.
Acta Physiologica Polonica
|
1955
|
tom 06
|
nr 3
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Social stress adapts signalling pathways involved in stimulation of the hypothalamic-pituitary-adrenal axis

100%
Bugajski J.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 3
4
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Role of prostaglandins in the stimulation of the hypothalamic-pituitary-adrenal axis by adrenergic and neurohormone systems

100%
Bugajski J.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 4
5

Gastric secretory receptors

88%
Bugajski J.
Acta Physiologica Polonica
|
1979
|
tom 30
|
nr 1
6

Receptory wydzielnicze żołądka

88%
Bugajski J.
Acta Physiologica Polonica
|
1980
|
tom 31
|
nr Supl.20[2]
7
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Zawartość histaminy w soku żołądkowym wydzielonym po pozornym karmieniu

63%
Bugajski J., Kaulbersz J.
Acta Physiologica Polonica
|
1960
|
tom 11
|
nr 5-6
8

Badania nad mechanizmem działania rezerpiny na wydzielanie żołądkowe

63%
Kaulbersz J., Bugajski J.
Acta Physiologica Polonica
|
1967
|
tom 18
|
nr 4
9

Prostaglandins and nitric oxide regulate adrenocortical response to vasopressin in stressed rats

63%
Gadek-Michalska A., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
10
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Wpływ rezerpiny na wydzielanie żołądkowe

63%
Kaulbersz J., Bugajski J.
Acta Physiologica Polonica
|
1960
|
tom 11
|
nr 5-6
11
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Wpływ czynników hormonalnych na ciśnienie i tętno w pracy fizycznej

63%
Bugajski J., Kaulbersz J.
Acta Physiologica Polonica
|
1955
|
tom 06
|
nr 3
12
Content available remote

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

63%
Bugajski J., Gadek-Michalska A.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
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.
13
Content available remote

Role of nitric oxide in the nicotine-induced pituitary-adrenocortical response

63%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 2
Nitric oxide (NO) is a major signaling molecule and biological mediator of the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the role of NO formed by endothelial (e), neuronal (n) and inducible (i) nitric oxide synthase (NOS) in the stimulatory effect of nicotine on the HPA axis in rats under basal conditions. Also possible interaction of NOS systems with endogenous prostaglandins (PG) in that stimulation was assessed. NOS and cyclooxygenase inhibitors were administered i.p. 15 min prior to nicotine (2, 5 mg/kg i.p.). Plasma ACTH and serum corticosterone levels were measured 1 h after nicotine injection. NOS blockers given alone did not markedly affect the resting ACTH and corticosterone levels. L-NAME (2-10 mg/kg), a broad spectrum NOS inhibitor considerably and dose dependently enhanced the nicotine-induced ACTH and corticosterone secretion. L-NNA (2 mg/kg) and 7-nitroindazole (7-NI 20 mg/kg), neuronal NOS inhibitors in vivo also significantly augmented the nicotine-induced ACTH and corticosterone levels. L-arginine greately impaired the nicotine-induced hormone responses and reversed the L-NNA elicited enhancement of the nicotine-evoked ACTH and corticosterone response. In contrast to the constitutive eNOS and nNOS antagonists, an inducible NOS antagonist guanethidine (50-100 mg/kg i.p.) did not substantially affect the nicotine-elicited pituitary-adrenocortical responses. Indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase blocker abolished the L-NAME and L-NNA-induced enhancement of the nicotine-evoked ACTH and corticosterone response. These results indicate that NO is an inhibitory mediator in the HPA axis activity. Inhibition of its generation by eNOS and nNOS significantly enhances the nicotine-induced HPA response. Under basal conditions iNOS is not involved in the nicotine-induced ACTH and corticosterone secretion. Prostaglandins play an obligatory role in the response of HPA axis to systemic nicotine administration.
14
Content available remote

Nitric oxide mediates the interleukin-1beta- and nicotine induced hypothalamic-pituitary-adrenocortical response during social stress

63%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 3
We investigated the role of nitric oxide (NO) in the interleukin 1b (IL-1ß) and nicotine induced hypothalamic-pituitary-adrenal axis (HPA) responses, and a possible significance of CRH and vasopressin in these responses under basal and social stress conditions. Male Wistar rats were crowded in cages for 7 days prior to treatment. All compounds were injected i.p., nitric oxide synthase (NOS) inhibitors, a-helical CRH antagonist and vasopressin receptor antagonist 15 min before IL-1ß or nicotine. Identical treatment received control non-stressed rats. Plasma ACTH and serum corticosterone levels were measured 1 h after IL-1ß or nicotine injection. L-NAME (2 mg/kg), a general nitric oxide synthase (NOS) inhibitor, considerably reduced the ACTH and corticosterone response to IL-1ß (0.5 µg/rat) the same extent in control and crowded rats. CRH antagonist almost abolished the nicotine-induced hormone responses and vasopressin antagonist reduced ACTH secretion. Constitutive endothelial eNOS and neuronal nNOS inhibitors substantially enhanced the nicotine-elicited ACTH and corticosterone response and inducible iNOS inhibitor, aminoguanidine, did not affect these responses in non-stressed rats. Social stress significantly attenuated the nicotine-induced ACTH and corticosterone response. In crowded rats L-NAME significantly deepened the stress-induced decrease in the nicotine-evoked ACTH and corticosterone response. In stressed rats neuronal NOS antagonist did not alter the nicotine-evoked hormone responses and inducible NOS inhibitor partly reversed the stress-induced decrease in ACTH response to nicotine. These results indicate that NO plays crucial role in the IL-1ß-induced HPA axis stimulation under basal and social stress conditions. CRH and vasopressin of the hypothalamic paraventricular nucleus may be involved in the nicotine induced alterations of HPA axis activity. NO generated by eNOS, but not nNOS, is involved in the stress-induced alterations of HPA axis activity by nicotine.
15
Content available remote

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

63%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
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.
16
Content available remote

Repeated handling, restraint, or chronic crowding impair the hypothalamic-pituitary-adrenocortical response to acute restraint stress

63%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
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.
17
Content available remote

Nitric oxide in the adrenergic- and CRH-induced activation of hypothalamic-pituitary-adrenal axis

63%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 2
In this report we investigated the effect of 7-nitroindazole (7-NI), a specific neuronal inhibitor of nitric oxide synthase (nNOS) and L-NAME, a nonselective NOS inhibitor upon the adrenergic- and CRH-induced stimulation of the hypothalamic-pituitary-adrenal axis in nonanesthetized rast. 7-NI given i.p. and L-NAME administered i.c.v. considerably reduced ACTH and corticosterone secretion induced by phenylephrine (30 µg i.c.v.), an alpha1-adrenergic receptor agonist. These inhibitors also diminished the HPA response to isoprenaline (20 µg i.c.v.), a nonselective ß-adrenergic receptor agonist, and i.c.v. L-NAME significantly lowered the ACTH and corticosterone response to clenbuterol (10 µg i.c.v.), a selective ß2-adrenergic agonist. L-NAME abolished the noradrenaline (NA), an alpha- and ß-receptor agonist-evoked ACTH and corticosterone response, which was reversed by pretreatment with i.p. L-arginine, an endogenous NO substrate. 7-NI abolished the stimulatory action of corticotropin-releasing hormone (CRH 1 µg/kg i.p.) on ACTH but not corticosterone secretion. L-NAME only moderately diminished the CRH-induced ACTH secretion, suggesting that a major part of the CRH-induced HPA axis activation is of neuronal origin. Dihydropyridine, nifedipine, a specific L-type Ca2+ channel blocker, inhibited significantly the CRH-induced ACTH and corticosterone response in rats exposed to 3 days crowding stress but not in rats under basal conditions. This finding indicates the strategic importance of Ca2+ influx into the pituitary corticotrops to meet increased secretory requirement under stressful conditions. Collectively, our results point to complex functional relationship between NO, adrenergic agents CRH and Ca2+ in the regulation of HPA axis activity.
18

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

51%
Glod R., Gadek-Michalska A., Olowska A., Bugajski J.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
19
Content available remote

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

51%
Gadek-Michalska A., Bugajski A. J., Bugajski J.
Journal of Physiology and Pharmacology
|
2008
|
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.
20

Nitric oxide and prostaglandins in the lipopolysaccharide-indiuced pituitary-adrenal response during stress

51%
Gadek-Michalska A., Spyrka J., Bugajski J.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
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