Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 11

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  AT1 receptor
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

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

100%
Matys T., Pawlak R., Kucharewicz I., Chabielska E., Buczko W.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 1
2
Content available remote

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

84%
Nakagiri A., Sunamoto M., Takeuchi K., Murakami M.
Journal of Physiology and Pharmacology
|
2010
|
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.
3

Immunochistochemical detection of angiotensin receptors AT1 and AT2 in adrenal tumors

84%
Pawlikowski M., Winczyk K., Sledz B.
Folia Histochemica et Cytobiologica
|
2008
|
tom 46
|
nr 1
51-55
4
Content available remote

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

84%
Rebas E., Lachowicz-Ochedalska A., Pawlikowski M.
Journal of Physiology and Pharmacology
|
2004
|
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.
5
Content available remote

Angiotensin II via AT1 receptor accelerates arterial thrombosis in renovascular hypertensive rats

84%
Kaminska M., Mogielnicki A., Stankiewicz A., Kramkowski K., Domaniewski T., Buczko W., Chabielska E.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 4
Although there are some in vitro evidence that angiotensin II (Ang II) may promote thrombosis, there is still no data concerning effect of Ang II on arterial thrombus formation. In the present study we have investigated the influence of Ang II on electrically induced arterial thrombosis in a common carotid artery of renovascular hypertensive rats. Furthermore, we examined if Ang II effect is mediated via AT1 receptor. We measured some coagulation and fibrinolytic parameters at the same time. Since platelets play crucial role in the initiation of arterial thrombosis their contribution in the mode of Ang II action was also determined. Intravenous infusion of Ang II caused significant increase in arterial thrombus weight, which was reversed by losartan, selective AT1 receptor antagonist. The prothrombotic effect of Ang II was accompanied by increase in haemostatic and decrease in fibrinolytic potential of rat plasma. While number of data has clearly demonstrated that Ang II can augment human platelets aggregation, at least in rats, platelets were not involved in the mechanism of Ang II action. Our study shows that Ang II via AT1 receptor accelerates arterial thrombosis in renovascular hypertensive rat, therefore may be considered as a risk factor of myocardial infarction or stroke.
6
Content available remote

Angiotensinogen and angiotensin-converting enzyme mRNA decrease and AT1 receptor mRNA and protein increase in epididymal fat tissue accompany age-induced elevation of adiposity and reductions in expression of GLUT4 and peroxisome proliferator-activated receptor (PPARgamma)

67%
Krskova K., Filipcik P., Zilka N., Olszanecki R., Korbut R., Gajdosechova L., Zorad S.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 4
7

CCN1 expression in interleukin-6 deficient mouse kidney in experimental model of heart failure

67%
Bonda T. A., Taranta A., Kaminski K. A., Dziemidowicz M., Litvinovich S., Kozuch M., Bialuk I., Chyczewski L., Winnicka M. M.
Folia Histochemica et Cytobiologica
|
2013
|
tom 51
|
nr 1
8

Atrial expression of the CCN1 and CCN2 proteins in chronic heart failure

67%
Bonda T. A., Kaminski K. A., Dziemidowicz M., Litvinovich S., Kozuch M., Hirnle T., Dmitruk I., Chyczewski L., Winnicka M. M.
Folia Histochemica et Cytobiologica
|
2012
|
tom 50
|
nr 1
9
Content available remote

Blockade of calcium channels and AT1 receptors prevents the hypertensive effect of calcilytic NPS 2143 in rats

67%
Rybczynska A., Jurska-Jasko A., Boblewski K., Lehmann A., Orlewska C.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 2
Calcilytics, antagonists of calcium receptor, decrease sensitivity of this receptor to plasma calcium concentration and increase parathyroid hormone (PTH) secretion. Moreover, it was recently indicated that calcilytic NPS 2143 induces hypertension in rats. This study tested whether the increase of mean arterial blood pressure (MAP) induced by NPS 2143 administration is mediated by calcium channel and angiotensin II type1 (AT1) receptor activity. Wistar rats were anaesthesized with Thiopental i.p. and infused i.v. with saline supplemented with the anaesthetic. Blood pressure was monitored continuously in the carotid artery. Effects of NPS 2143 administered i.v. as bolus on MAP in the presence and absence of felodypine and losartan were investigated. Both, felodipine and losartan pretreatment provoked a persistent MAP decrease by 18±3 and 14±3 mmHg, respectively. Infusion of NPS 2143 at 1 mg/kg b.w. confirmed hypertensive activity of calcilytic and increased blood pressure for 21±4 mmHg. In contrast, administration of NPS 2143 in felodipine as well as in losartan pretreated rats did not change MAP as compared to felodipine/control and losartan/control groups, respectively. Our study indicated that both the blockade of calcium channels and the AT1 receptor activity prevented the hypertensive effect of calcilytic NPS 2143. This finding might be particularly important in understanding the mechanisms that mediated blood pressure changes related to the activity of calcium receptor.
10
Content available remote

Cardiovascular effects of the combination of levosimendan and valsartan in hypertensive Dahl/Rapp rats

67%
Biala A., Finckenberg P., Korpi A., Loytainen M., Martonen E., Levijoki J., Mervaala E.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 3
Hypertension is the main risk factor for left ventricular hypertrophy and development of diastolic heart failure. There is no yet treatment, which can effectively reduce mortality in patients suffering from heart failure with preserved systolic function. We tested whether the calcium sensitizer levosimendan and the AT1-receptor antagonist valsartan could protect from salt-induced hypertension, cardiovascular mortality and heart failure in Dahl/Rapp salt-sensitive rats fed for 7 weeks with a high salt diet (8% NaCl). Levosimendan (1 mg/kg/day via drinking water) and valsartan (30 mg/kg in the food) monotherapies and their combination prevented mortality in Dahl/Rapp rats. The drug combination evoked an additive effect on blood pressure, cardiac hypertrophy, cardiomyocyte cross-sectional area, target organ damage and myocardial ANP mRNA expression. There was a close correlation between systolic blood pressure and cardiac hypertrophy, cardiac and renal damage. As compared to Dahl/Rapp controls kept on low-salt diet (NaCl 0.3%). The high salt rats exhibited impaired diastolic relaxation as assessed by isovolumic relaxation time. Levosimendan alone and in combination with valsartan, improved diastolic relaxation without significantly improving systolic function. Our findings are evidence for an additive effect between levosimendan and valsartan on blood pressure and a blood pressure- dependent protection against the development of salt-induced target organ damage. The present study also demonstrates that levosimendan, alone or in combination with valsartan, can correct diastolic dysfunction induced by salt-dependent hypertension.
11
Content available remote

Vascular effects of COX inhibition and AT1 receptor blockade in transgenic rats harboring mouse renin-2 gene

67%
Cheng Z. J., Tikkanen I., Vapaatalo H., Mervaala E. M. A.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
Ang II-induced endothelial dysfunction is associated with perivascular inflammation and increased superoxide production in the vascular wall. The present study examined the role of cyclo-oxygenase (COX)-synthetized eicosanoids in the pathogenesis of Ang II-induced endothelial dysfunction in transgenic rats harboring mouse renin-2 gene (mREN2 rats). Five-to-six-week-old, heterozygous mREN2 rats received the following drug regimens for 8 weeks: 1) vehicle, 2) cyclo-oxygenase-2 (COX-2) inhibitor (MF-tricyclic [3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl) phenyl)-2(5H)-furanone], 14 mg/kg p.o.), 3) COX-l/COX-2 inhibitor (sulindac, 14 mg/kg p.o.), 4) angiotensin II receptor antagonist (losartan 40 mg/kg p.o.). Normotensive Sprague Dawley (SD) rats served as controls. In vitro vascular responses of the descending aorta and renal artery were studied using organ bath system. mREN2 rats developed pronounced hypertension which was associated with impaired endothelium-dependent and endothelium-independent vascular relaxations in the aorta. In contrast, the relaxation responses of the renal arteries remained largely unchanged in mREN2 rats. Urinary NOx excretion, a marker of total body NO generation, was also decreased in mREN2 rats. Neither non-selective COX inhibitor sulindac nor COX-2 selective MF-tricyclic were capable of preventing Ang II- induced hypertension or endothelial dysfunction in mREN2 rats, whereas ATi receptor antagonist losartan completely normalized blood pressure, vascular relaxation responses as well as urinary NOx excretion. Our findings indicate that NO synthesis and/or bioavailability as well as the sensitivity of arterial smooth muscle cells to NO are decreased in mREN2 rats. The present study also demonstrated that COX does not play a central role in the pathogenesis of Ang II-induced endothelial dysfunction in mREN2 rats.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.