Wyniki wyszukiwania

1

Effect of angiotensin II on protein phosphorylation in PC12 cell line

100%

Zielinski B., Seweryn E., Berdowska I., Ceremuga I.

Folia Histochemica et Cytobiologica. Supplement

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2001

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tom 39

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nr 1

2

The modulatory effect of flavonoid glycosides on angiotensin II stimulated PC 12 cells

100%

Zielinski B., Berdowska I., Seweryn E., Ceremuga I., Chwilkowska A., Fecka I., Banas T.

Cellular and Molecular Biology Letters

|

2002

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tom 07

|

nr Suppl.

3

The physiological significance of the alternative pathways of angiotensin II production

88%

Kramkowski K., Mogielnicki A., Buczko W.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

Although the use of angiotensin converting enzyme inhibitors (ACE-Is) in clinical practice brought the great chance to recognize the RAS role in the physiology and pathology, there are still many questions which we cannot answer. This article reviews actually known pathways of angiotensin II (Ang II) and other peptides of renin-angiotensin system (RAS) production and their physiological significance. The various carboxy- and aminopeptidases generate a range of peptides, like Ang II, Ang III, Ang IV, Ang-(1-7) and Ang-(1-9) possessing their own and known biological activity. In this issue especially the alternative pathways of Ang II synthesis involving enzymes other than angiotensin-converting enzyme (ACE) are discussed. We present many evidences for the significance of a new pathway of Ang II production. It has been clearly shown that Ang I may be converted to Ang-(1-9) by angiotensin-converting enzyme-related carboxypeptidase (ACE-2) and then into Ang II in some tissues, but the enzymes responsible for this process are unknown till now. Although there are many data proving the existence of alternative pathways of Ang II production, we can still block only ACE and angiotensin receptor 1 (AT1) in clinical practice. It seems that a lot needs to be done before we can wildly complexively control RAS and treat more effectively cardiovascular disorders such as hypertension or heart failure.

4

The effect of losartan on Ang II and Ang IV-induced changes in tyrosine protein kinase activity in rat pituitary in vitro

75%

Rebas E., Lachowicz A.

Cellular and Molecular Biology Letters

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2002

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tom 07

|

nr Suppl.

5

Effects of angiotensin II and its receptor antagonists on motor activity and anxiety in rats

75%

Braszko J. J., Kulakowska A., Winnicka M. M.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 2

The neuropeptide angiotensin II (Ang II) has been recently found to be involved in cognitive processes. Both AT1 and AT2 angiotensin receptors seem to mediate this action. However, unspecific behavioural effects of the peptide, particularly motor and emotional, appear to influence the interpretation of cognition-oriented tests and contribute to considerable differences in opinions of various authors on the subject. In this study, aimed specifically at the assessment of these effects, we found small and insignificant changes in motor performance measured in open field after intracebroventricular injections of Ang II and its receptor subtype-specific antagonists; losartan (AT1) and PD 123319 (AT2). However, Ang II was found to increase substantially anxiety measured in elevated 'plus' maze and impair motor coordination measured in 'chimney test'. Interestingly, both antagonists abolished Ang II generated anxiety and only losartan counteracted impaired motor coordination caused by the peptide. The AT2 receptor antagonist PD 123319 impairing motor coordination on its own, nonetheless partly diminished that caused by Ang II. Therefore it appears safe to conclude that mood but not motor effects of AT1 and AT2 receptor affecting drugs may significantly bias interpretation of the cognition - oriented tests on these drugs.

6

Angiotensins II and IV modulate adrenocortical cell proliferation in ovariectomized rats

75%

Siejka A., Melen-Mucha G., Mucha S. A., Pawlikowski M.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 3

Effects of angiotensins II (AngII), angiotensin IV (AngIV, 3-8 fragment of angiotensin II) and losartan (an antagonist of angiotensin receptor type 1) on the proliferation of adrenocortical cells in ovariectomized rats have been studied. The incorporation of bromodeoxyuridine (BrdU) into cell nuclei was used as an index of cell proliferation. AngIV decreased BrdU labeling index mainly in the reticularis zone and losartan (Los) was able to partially reverse this inhibitory effect of AngIV. AngII had no effect on the adrenocortical cell proliferation when given alone, however Los given simultaneously diminished BrdU incorporation into nuclei of glomerulosa and reticularis zones as compared with AngII. These findings suggest that AngII and AngIV modulate adrenocortical cell proliferation in ovariectomized rats.

7

The eicosanoid factor: a determinant of individuality of nephron segments

75%

McGiff J. C., Ferreri N. R., Carroll M. A.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Nephron function is segmented; each segment has characteristic transport mechanisms and individual eicosanoid profiles. The transport function of the medullary thick ascending limb of Henle's loop (mTAL) establishes the osmolar gradient upon which extra cellular fluid volume (ECFV) conservation depends. The overriding importance of the mTAL to regulation of ECFV is evident in the diuretic- natriuretic potency of furosemide-like agents which target the mTAL. Results: The mTAL has been shown to be heavily invested with cytochrome P450 monooxygenases (CYP), chiefly / -1 hydroxylase activity, that generate 19- and 20-hydroxyeicosatetraenoic acid (HETEs). However, displacement of w hydroxylase by an inducible cyclooxygenase mechanism (COX-2) can be effected by several interventions: long-term infusion of angiotensin II (ANG II), adrenalectomy and elevated extracellular Ca2+ concentrations. This switching mechanism (CYP ³ COX- 2) has been shown to be dependent on activation of tumor necrosis factor alpha (TNFalpha) by ANG II. It represents a long-term adaptive mechanism of the mTAL with production of PGE2 whereas in the short-term, ANG II increases 20-HETE synthesis by the mTAL. The effect of Ca2+ on mTAL eicosanoid-related mechanisms provides an explanation for the natriuretic response to hypercalcemia and diminished ability to concentrate urine. Conclusion: The expression of COX-2 in the TAL has been linked to activation of the renin-angiotensin system, glucocorticoid deficiency and hypercalcemia, all of which operate through a mechanism in which production of TNFa by the TAL is pivotal.

8

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Hypotensive effect of angiotensin II after AT1-receptor blockade with losartan

75%

Matys T., Pawlak R., Kucharewicz I., Chabielska E., Buczko W.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 1

9

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

63%

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

|

2010

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tom 61

|

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.

10

Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II

63%

Nakagiri A., Sunamoto M., Takeuchi K., Murakami M.

Journal of Physiology and Pharmacology

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2010

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tom 61

|

nr 2

Reactive oxygen species are known to be derived from NADPH oxidase in several tissues. Angiotensin II was suggested to be involved in the activation of NADPH oxidase; however, its role in the gastric mucosa is unclear. We examined the roles of angiotensin II receptor and NADPH oxidase in ischemia/reperfusion-induced gastric damage in rats. Under urethane anesthesia, male Sprague-Dawley rat stomachs were mounted in an ex-vivo chamber, had 100 mM HCl applied to them, and then a catheter was passed through the femoral vein. Ischemia/reperfusion was accompanied by blood collection and reperfusion through the catheter. Losartan, candesartan, valsartan, which are AT1 receptor blockers (ARB); PD123319, an AT2 receptor blocker; enalapril, an ACE inhibitor; or diphenylene iodonium, a NADPH oxidase inhibitor, was given i.v. 10 mins, and ß-NADPH, a NADPH oxidase substrate, was given i.v. 5 mins before reperfusion. The gastric damage by ischemia/reperfusion was attenuated by treatment with any of ARB or enalapril, but was not affected by PD123319. The increase in gastric H2O2 production and microvascular permeability by ischemia/reperfusion was also suppressed by treatment with any of ARB or enalapril. In rat gastric mucosa, the NADPH oxidase subunit p47phox was detected. Additionally, diphenylene iodonium had similar effects to ARB against ischemia/reperfusion-caused gastric damage, increased H2O2 production, and microvascular permeability. Ischemia/reperfusion activated NADPH oxidase in the gastric mucosa, and the activation was significantly attenuated by treatment with losartan or diphenylene iodonium. These results suggest that ischemia/reperfusion generated reactive oxygen species are derived from NADPH oxidase activation via AT1 receptor in rat stomachs.

11

Heart rate reduction with ivabradine in the early phase of atherosclerosis is protective in the endothelium of ApoE-deficient mice

63%

Aquila G., Morelli M. B., Vieceli Dalla Sega F., Fortini F., Nigro P., Caliceti C., Ferracin M., Negrini M., Pannuti A., Bonara M., Pinton P., Ferrari R., Rizzo P.

Journal of Physiology and Pharmacology

|

2018

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tom 69

|

nr 1

12

The time-dependent alteration of anti-diuretic hormone system in hindlimb unloaded rats

63%

Chung S. Y., Kim S. K., Hong C. W., Oh K. W., Kim K. T., Sul J. G., Chung J. W., Kwon M. S.

Journal of Physiology and Pharmacology

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2012

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tom 63

|

nr 1

13

Sex-specific response of renal Na,K-ATPase to prenatal angiotensin 2 exposure and increased salt intake in offspring

63%

Jagmasevic-Mezesova L., Svitok P., Kalocayova B., Zeman M., Vrbjar N.

Journal of Physiology and Pharmacology

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2018

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tom 69

|

nr 1

14

Regulation of cGMP synthesis in cultured podocytes by vasoactive hormones

63%

Lewko B., Golos M., Latawiec E., Angielski S., Stepinski J.

Journal of Physiology and Pharmacology

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2006

|

tom 57

|

nr 4

The podocytes are highly differentiated cells playing a key role in glomerular filtration. Vasoactive factors including angiotensin II (Ang II) and cyclic guanosine 5' monophosphate (cGMP) are synthesized by these cells upon stimulation as well as in the basal state. In this study we have tested whether angiotensin II affects the total synthesis of cGMP in primary culture of rat podocytes. The cells were stimulated with atrial natriuretic peptide (ANP) and/or a nitric oxide (NO) donor, S-nitroso-N-acetyl penicillamine (SNAP), in the absence or presence of Ang II. The cGMP synthesis was determined by radioimmunoassay (RIA). ANP or SNAP alone increased the cGMP synthesis in podocytes although the effects were not additive unless Ang II was present in the medium. Ang II suppressed the ANP-dependent cGMP synthesis whereas SNAP-dependent cGMP production remained unaffected. These effects were prevented by a non-specific antagonist of Ang II receptors (AT), saralasin. Adversely, PD123319, a specific inhibitor of AT2 receptors, augmented inhibition of ANP-dependent and enhanced the NO-dependent cGMP production. Probenecid, an inhibitor of cGMP extrusion from the cells, suppressed the cGMP generation by both ANP and SNAP. We conclude that cGMP synthesis in cultured podocytes is modulated by angiotensin II and that two adversely acting receptors, AT1 and AT2 are involved in this effect. Additionally, production of cGMP might be intrinsically inhibited by cGMP accumulating inside the cells.

15

Angiotensin IV stimulates the activity of tyrosine kinases in rat anterior pituitary gland acting via AT1-like receptors?

63%

Rebas E., Lachowicz-Ochedalska A., Pawlikowski M.

Journal of Physiology and Pharmacology

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2004

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tom 55

|

nr 1,1

Angiotensin II (Ang II) is known to modulate tyrosine kinases (PTKs) activity in pituitary tumor cells. It is known that AngII is acting via AT1 receptors in many tissues. The aim of this study was to see whether 3-8 fragment of AngII, called angiotensin IV (AngIV) has a similar effect on tyrosine kinase activity in normal pituitary gland and what type of angiotensin receptor is involved in this process. The homogenates of normal rat pituitaries was a source of enzymes. The PTKs activity was determined using the synthetic substrate poly GluTyr and -32P-ATP. Ang IV was found to increase the PTK activity in the rat anterior pituitary tissue, with the maximal effect at concentration of 10-10M. AngII was ineffective at all concentrations studied. Losartan, a selective AT1 receptor blocker, added together with Ang IV abolished the effect of the latter, however losartan diminished also the PTK activity when applied together with Ang II, but only when it was added immediately before, but not after, the addition of Ang II. The involvement of a non-classic AT1-like receptor is suggested.

16

Kaempferol, but not resveratrol inhibits angiotensin converting enzyme

63%

Olszanecki R., Bujak-Gizycka B., Madej J., Suski M., Wolkow P. P., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

|

2008

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tom 59

|

nr 2

Inhibition of angiotensin converting enzyme (ACE) has proved to be beneficial in the treatment of various cardiovascular disorders. The aim of this study was to evaluate ACE inhibitory potential of two polyphenolic compounds with different structures: resveratrol (present in high quantities in French wine) and kaempferol (abundant in greens), using method of liquid chromatography coupled with electrospray ionization mass spectrometry (LC-ESI-MS) for ex vivo measurement of angiotensin I to angiotensin II conversion by ACE in aortic tissue of Wistar-Kyoto rats. In this setting, kaempferol (10-30-100 µM), but not resveratrol (10-30-100 µM) appeared to inhibit dose-dependently conversion of Ang I to Ang II. Although the mechanism of ACE inhibition by kaempferol remains to be elucidated, this observation may help in search or designing of new classes of ACE inhibitors.

17

Enhanced food and water intake in renin transgenic rats

63%

Szczepanska-Sadowska E., Paczwa P., Dobruch J.

Journal of Physiology and Pharmacology

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2003

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tom 54

|

nr 1

In short term experiments angiotensin II (Ang II) is a potent stimulant of thirst, however it is not known whether prolonged activation of the renin-angiotensin system is associated with chronic alteration of water or food intake. Renin transgenic rats TGRmRen(2)27 (TGR) exhibit significant elevation of AngII in the brain regions involved in regulation of body fluid balance. The purpose of the present study was to find out whether TGR rats manifest also different water (WI) and food (FI) intake and renal excretory functions in comparison to their parent Sprague Dawley (SD) strain. To this end 24h WI and FI as well as urine excretion (Vu) and urinary outputs of solutes (Cosm), sodium (UNaV) and potassium (UKV) were compared under baseline conditions in 16 TGR and 15 SD rats having free access to water and food. In 15 TGR and 17 SD rats effect of 24h dehydration on water intake was investigated. Under baseline conditions TGR rats consumed significantly greater amount of food and water than SD rats. Vu, UNaV and UKV were not significantly different in both strains. Cumulative water intakes in SD and TGR rats subjected to 24h dehydration did not differ. The results reveal that under baseline conditions TGR rats manifest greater food and water intakes than SD rats whereas stimulation of thirst by water deprivation is similar in both strains. The results suggest that the ingestive behavior may be chronically altered by upregulation of the renin-angiotensin system.

18

Pathways of glomerular toxicity of cyclosporine-A: an "in vitro" study

63%

Castello L., Sainaghi P. P., Bergamasco L., Letizia C., Bartoli E.

Journal of Physiology and Pharmacology

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2005

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tom 56

|

nr 4

Background/Aims. Knowledge of renal toxicity of cyclosporine-A (CyA) is clouded by multiple effects on different glomerular and tubular cells and on kidney and systemic hemodynamics. To focus on glomerular action of CyA we used glomeruli isolated in vitro, with the aim of dissecting the effects on recruitment of glomerular vasoconstricting systems, like endothelin-1 (ET) and angiotensins (AI and AII). Methods. We studied the pathways of CyA damage on pig glomeruli isolated in vitro with the technique of sieving through mesh filters of different sizes, and incubated in an appropriate culture medium. The supernatant was sampled at different time intervals to measure ET, AI and AII concentrations upon addition of ET 10-12 or CyA 4·10-7 M, with or without either selective endothelin receptor A (ETA) or B (ETB), or unselective ETA-ETB receptor inhibitors. Results. CyA increased ET concentration (from 9.7±0.3 to 11.4±0.4 pg·ml-1, p<0.002), and the added ET released AI in the medium (from 26.6±4.7 to 39.1±4.6 pg·ml-1, p<0.05) when ETB receptors were blocked. In contrast, CyA stimulated angiotensins release independent of ET receptors blockade, hence, irrespective of ET concentration in the medium, from 26.6±4.7 to 38.0±2.1 pg·ml-1 for AI, p<0.05, and from 12.3±1.0 to 14.8±0.9 pg·ml-1 for AII, p<0.05. Conclusion. CyA releases ET and angiotensins independently by a direct action. Glomerular CyA toxicity might be mediated by recruitment of vasoconstricting peptides and modulated by relative ETA and ETB receptor occupancy.

19

Influence of redox agents on activity of protein tyrosine phosphatases and kinases in human aortic endothelial cells

63%

Zielinski B., Seweryn E., Banas T.

Cellular and Molecular Biology Letters

|

1999

|

tom 04

|

nr 2

20

CGP 42112A abolishes facilitation of recognition caused by angiotensin II and angiotensin II[3-7] in rats

63%

Braszko J. J., Kulakowska A., Winnicka M. M., Karwowska-Polecka W.

Acta Neurobiologiae Experimentalis

|

1997

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tom 57

|

nr 3

Ograniczanie wyników

Effect of angiotensin II on protein phosphorylation in PC12 cell line

The modulatory effect of flavonoid glycosides on angiotensin II stimulated PC 12 cells

The physiological significance of the alternative pathways of angiotensin II production

The effect of losartan on Ang II and Ang IV-induced changes in tyrosine protein kinase activity in rat pituitary in vitro

Effects of angiotensin II and its receptor antagonists on motor activity and anxiety in rats

Angiotensins II and IV modulate adrenocortical cell proliferation in ovariectomized rats

The eicosanoid factor: a determinant of individuality of nephron segments

Hypotensive effect of angiotensin II after AT1-receptor blockade with losartan

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

Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II

Heart rate reduction with ivabradine in the early phase of atherosclerosis is protective in the endothelium of ApoE-deficient mice

The time-dependent alteration of anti-diuretic hormone system in hindlimb unloaded rats

Sex-specific response of renal Na,K-ATPase to prenatal angiotensin 2 exposure and increased salt intake in offspring

Regulation of cGMP synthesis in cultured podocytes by vasoactive hormones

Angiotensin IV stimulates the activity of tyrosine kinases in rat anterior pituitary gland acting via AT1-like receptors?

Kaempferol, but not resveratrol inhibits angiotensin converting enzyme

Enhanced food and water intake in renin transgenic rats

Pathways of glomerular toxicity of cyclosporine-A: an "in vitro" study

Influence of redox agents on activity of protein tyrosine phosphatases and kinases in human aortic endothelial cells

CGP 42112A abolishes facilitation of recognition caused by angiotensin II and angiotensin II[3-7] in rats