Wyniki wyszukiwania

1

The effect of adrenergic receptors on ionic transport in the skin of a frog Rana esculenta L.

100%

Kosik-Bogacka D., Tyrakowski T.

Zoologica Poloniae

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2001

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tom 46

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nr 1-4

2

Carvedilol and adrenergic agonists suppress the lipopolysaccharide-induced NO production in RAW 264.7 macrophages via the adrenergic receptors

86%

Pekarova M., Kralova J., Kubala L., Ciz M., Papezikova I., Macickova T., Pecivova J., Nosal R., Lojek A.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 1

143-150

The interaction of adrenergic agonists and/or antagonists with the adrenergic receptors expressed on immunologically active cells including macrophages plays an important role in regulation of inflammatory responses. Our study investigated the effects of carvedilol, a unique vasodilating b-adrenergic antagonist, and endogenous adrenergic agonists (adrenalin, noradrenalin, and dopamine) and/or antagonists (prazosin, atenolol) on lipopolysaccharide-stimulated nitric oxide (NO) production from murine macrophage cell line RAW 264.7. The production of NO was determined as the concentration of nitrites in cell supernatants (Griess reaction) and inducible nitric oxide synthase (iNOS) protein expression (Western blot analysis). Scavenging properties against NO were measured electrochemically. Carvedilol in a concentration range of 1, 5, 10 and 25 µM inhibited iNOS protein expression and decreased the nitrite concentration in cell supernatants. Adrenalin, noradrenalin or dopamine also inhibited the iNOS protein expression and the nitrite accumulation. Prazosine and atenolol prevented the effect of both carvedilol and adrenergic agonists on nitrite accumulation and iNOS expression in lipopolysaccharide-stimulated cells. These results, together with the absence of scavenging properties of carvedilol against NO, imply that both carvedilol and adrenergic agonists suppress the lipopolysaccharide-evoked NO production by macrophages through the activation and modulation of signaling pathways connected with adrenergic receptors.

3

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

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

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

86%

Bugajski J., Gadek-Michalska A., Glod R., 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 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.

7

Relation of adrenergic receptors, which have roles in gastroprotective and anti-inflammatory effect of adrenal gland hormones, with cyclooxygenase enzyme levels in rats

72%

Suleyman H., Dursun H., Bilici M., Cadirci E., Halici Z., Gulaboglu M., Albayrak F.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 4

129-134

Background and Aims: COX-2 enzyme inhibition is responsible for the anti-inflammatory effects of NSAIDs, COX-1 for their effects upon the gastrointestinal system (GIS), along with other side effects. We investigated the relationship between COX levels and those adrenergic receptors known to play a role in gastroprotection and anti-inflammatory activity. Method: The effects of adrenaline and prednisolone on gastric COX-1 and COX-2 levels in both intact and adrenalectomized rats treated with doxazosin, yohimbine, propranolol, and metoprolol were determined. Results: We found that adrenaline increases COX-1 levels in the gastric tissue of both intact and adrenalectomized rats by stimulating -2 receptors. Adrenaline decreases COX-2 levels by stimulating ß-2 adrenergic receptors. Prednisolone inhibits both COX-1 and COX-2 in the gastric tissue of intact rats. In adrenalectomized rats, prednisolone increases gastric COX-1 by stimulating -2 receptors, and decreases COX-2 levels by stimulating ß-2 receptors. Conclusion: Prednisolone cannot bind to a adrenergic receptors in the presence of adrenaline (intact rats) but, in its absence (adrenalectomy), binds to -2 receptors, and stimulates them more effectively than adrenaline, suggesting a direct relationship between -2 adrenergic receptors and COX-1 levels, whereas ß-2 receptors are directly related to COX-2 levels.

8

Involvement of the monoaminergic system in the antidepressant-like activity of chromium chloride in the forced swim test

72%

Piotrowska A., Siwek A., Wolak M., Pochwat B., Szewczyk B., Opoka W., Poleszak E., Nowak G.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 4

9

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

10

Noradrenaline - and glutamate - induced taurine release from bulk isolated adult rat astrocytes

72%

Puka M., Albrecht J., Lazarewicz J. W.

Acta Neurobiologiae Experimentalis

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1992

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tom 52

|

nr 1

11

Multifactorial mediation of post norepinephrine induced intestinal hyperemia

72%

Remak G., Hottenstein O. D., Jacobson E. D.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

12

Catecholamines reduce transient receptor potential vanilloid type 1 desensitization in cultured dorsal root ganglia neurons

58%

Filippi A., Caruntu C., Gheorghe R. O., Deftu A., Amuzescu B., Ristoiu V.

Journal of Physiology and Pharmacology

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2016

|

tom 67

|

nr 6

13

Catecholaminergic regulation of the hypothalamic-pituitary-adrenocortical activity

58%

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

|

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.

14

The neuromodulation aspects of ischaemic myocardium: the importance of cholinergic system

58%

Gajewski M., Moutiris J. A., Maslinski S., Ryzewski J.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 2

15

Adrenergic regulation of the hypothalamic-pituitary-adrenal axis under basal and social stress conditions

58%

Bugajski J., Gadek-Michalska A., Olowska A., Borycz J., Glod R., Bugajski A. J.

Journal of Physiology and Pharmacology

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1995

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tom 46

|

nr 3

16

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

51%

Bugajski J.

Journal of Physiology and Pharmacology

|

1996

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tom 47

|

nr 4

Ograniczanie wyników

The effect of adrenergic receptors on ionic transport in the skin of a frog Rana esculenta L.

Carvedilol and adrenergic agonists suppress the lipopolysaccharide-induced NO production in RAW 264.7 macrophages via the adrenergic receptors

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

The influence of indomethacin on the ACTH secretion induced by central stimulation of adrenergic receptors

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

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

Relation of adrenergic receptors, which have roles in gastroprotective and anti-inflammatory effect of adrenal gland hormones, with cyclooxygenase enzyme levels in rats

Involvement of the monoaminergic system in the antidepressant-like activity of chromium chloride in the forced swim test

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

Noradrenaline - and glutamate - induced taurine release from bulk isolated adult rat astrocytes

Multifactorial mediation of post norepinephrine induced intestinal hyperemia

Catecholamines reduce transient receptor potential vanilloid type 1 desensitization in cultured dorsal root ganglia neurons

Catecholaminergic regulation of the hypothalamic-pituitary-adrenocortical activity

The neuromodulation aspects of ischaemic myocardium: the importance of cholinergic system

Adrenergic regulation of the hypothalamic-pituitary-adrenal axis under basal and social stress conditions

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