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4-aminopyridine induces positive lusitropic effects and prevents the negative inotropic action of phenylephrine in the rat cardiac tissue subjected to ischaemia

100%

Kocic I., Dworakowska D., Dworakowski R.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 3

2

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

84%

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 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.

3

Comparison of the effect of alpha1- and alpha2-adrenoceptor agonists and antagonists on muscle contractility of the rabbit abdominal aorta in vitro

84%

Gnus J., Rusiecka A., Czerski A., Zawadzki W., Witkiewicz W., Hauzer W.

Folia Biologica

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2013

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tom 61

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nr 1-2

4

Beta-adrenergic antagonists influence abdominal aorta contractility by mechanisms not involving beta-adrenergic receptors

84%

Hauzer W., Bujok J., Czerski A., Rusiecka A., Pecka E., Gnus J., Zawadzki W., Witkiewicz W.

Folia Biologica

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2014

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tom 62

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nr 3

5

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

84%

Pecanha F. M., Wiggers G. A., Briones A. M., Perez-Giron J. V., Miguel M., Garcia-Redondo A. B., Vassallo D. V., Alonso M. J., Salaices M.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 1

29-36

We have previously demonstrated that chronic exposure to low-dose of mercury induced endothelial dysfunction and increased vasoconstrictor responses. The aim of this work was to investigate if mercury exposure alters contractile prostanoids production from cyclooxygenase-2 (COX-2) and its contribution to phenylephrine responses. For this, aortic segments from 3-month old Wistar rats daily treated with HgCl2 (1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m.) or vehicle for 30 days were used. Mercury treatment did not affect systolic blood pressure but increased phenylephrine-induced vasoconstriction. The non selective COX inhibitor, indomethacin (10 µmol/l) reduced the response to phenylephrine more in aortic segments from mercury-treated than control rats. The selective COX-2 inhibitor NS 398 (1 µmol/l), the thromboxane A2/prostaglandin H2 receptor (TP) antagonist SQ 29,548 (1 µmol/l), the TXA2 synthase inhibitor furegrelate (1 µmol/l), the EP1 receptor antagonist SC 19220 (1 µmol/l) and the AT1 receptor antagonist losartan (10 µmol/l) reduced phenylephrine response only in vessels from mercury-treated rats. TXA2 and PGE2 levels were greater in the incubation medium of vessels from treated than untreated rats; NS 398 decreased these levels only in the mercury group. COX-2 protein was localized in adventitial and endothelial cells. Aortic COX-2 mRNA expression and plasma angiotensin converting enzyme activity were greater in mercury-treated rats. These results suggest that treatment with low doses of mercury increases the release of COX-2-derived vasoconstrictor prostanoids and its participation in phenylephrine responses. The increased activation of the renin-angiotensin system after mercury treatment might be associated to this increased COX-2 activity.

6

Vasodilatory effect and endothelial integrity in papaverine- and milrinone-treated human radial arteries

84%

Rudzinski P., Wegrzyn P., Lis G. J., Piatek J., Konstanty-Kalandyk J., Nosalski R., Mikolajczyk T., Jasinska M., Pyka-Fosciak G., Guzik T., Litwin J. A., Korbut R., Sadowski J.

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 1

7

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

84%

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

|

nr 2

8

Central nervous stimuli increase duodenal bicarbonate secretion by release of mucosal melatonin

84%

Sjoblom M., Flemstrom G.

Journal of Physiology and Pharmacology

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2001

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tom 52

|

nr 4,1

A number of common diseases in humans, including gastroduodenal ulcer and irritable bowel syndrome, show circadian rhythms in pain and discomfort. The neurohormone melatonin is released from enterochromaffin cells in the intestinal mucosa and from the pineal gland but its role in gastrointestinal function is largely unknown. We have studied the involvement of melatonin in stimulation of the mucosa-protective alkaline secretion by the duodenal mucosa. A 12-mm segment of proximal duodenum with an intact blood supply was cannulated in situ in anesthetized rats and duodenal HCO3– secretion titrated by pH-stat. Duodenal close intra-arterial infusion of melatonin or the full agonist 2-iodo-N-butanoyl- 5-methoxytryptamine significantly increased the secretion and pretreatment with the melatonin (predominantly MT2-receptor specific) antagonist luzindole almost abolished the response. Intracerebroventricular (i.c.v.) infusion of the alpha1-adrenoceptor agonist phenylephrine (12.2 µmol kg-1·h-1 ) caused an up to fivefold increased in the alkaline secretion and the melatonin antagonist luzindole or cutting all peri-carotid nerves abolished the duodenal secretory response to i.c.v. phenylephrine. Peripheral melatonin thus stimulates duodenal mucosal HCO3 – secretion and endogenous melatonin, very likely released from mucosal enterochromaffin cells, is involved in mediating neural stimulation of the secretion.

9

Mantidis ootheca induces vascular relaxation through PI3K/Akt-mediated nitric oxide-cyclic GMP-protein kinase G signaling in endothelial cells

67%

Kim H. Y., Lee Y. J., Han B. H., Yoon J. J., Ahn Y. M., Hong M. H., Tan R., Kang D. G., Lee H. S.

Journal of Physiology and Pharmacology

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2017

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tom 68

|

nr 2

10

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

67%

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

11

The influence of experimental hyperlipidemia on the time course of contractility during simulated ischaemia and reperfusion and responsiveness to phenylephrine of rat heart papillary muscle

67%

Kocic I., Dworakowska D., Konstanski Z., Dworakowski R.

Journal of Physiology and Pharmacology

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1998

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tom 49

|

nr 3

12

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

59%

Bugajski J.

Journal of Physiology and Pharmacology

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1996

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tom 47

|

nr 4

Ograniczanie wyników

4-aminopyridine induces positive lusitropic effects and prevents the negative inotropic action of phenylephrine in the rat cardiac tissue subjected to ischaemia

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

Comparison of the effect of alpha1- and alpha2-adrenoceptor agonists and antagonists on muscle contractility of the rabbit abdominal aorta in vitro

Beta-adrenergic antagonists influence abdominal aorta contractility by mechanisms not involving beta-adrenergic receptors

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

Vasodilatory effect and endothelial integrity in papaverine- and milrinone-treated human radial arteries

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

Central nervous stimuli increase duodenal bicarbonate secretion by release of mucosal melatonin

Mantidis ootheca induces vascular relaxation through PI3K/Akt-mediated nitric oxide-cyclic GMP-protein kinase G signaling in endothelial cells

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

The influence of experimental hyperlipidemia on the time course of contractility during simulated ischaemia and reperfusion and responsiveness to phenylephrine of rat heart papillary muscle

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