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

100%

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.

Antithrombotic effect of tissue and plasma type angiotensin converting enzyme inhibitors in experimental thrombosis in rats

84%

Wojewodzka-Zelazniakowicz M., Chabielska E., Mogielnicki A., Kramkowski K., Karp A., Opadczuk A., Domaniewski T., Malinowska-Zaprzalka M., Buczko W.

Journal of Physiology and Pharmacology

2006

tom 57

nr 2

This study compared the antihrombotic effect of plasma angiotensin converting enzyme inhibitors (ACE-Is): captopril (CAP), enalapril (ENA) and Tissue ACE-Is: perindopril (PER), quinapril (QUIN) in experimental venous and arterial thrombosis. Normotensive Wistar rats were treated p.o. with CAP (75 mg/kg), ENA (20 mg/kg), PER (2 mg/kg) and QUIN (3 mg/kg) for 10 days. The influence of ACE-Is on coagulation and fibrinolytic systems as well as platelet function was evaluated. The hypotensive effect of ACE-Is was equal in all groups. QUIN mantained the final carotid blood flow at the highest value in comparison to PER and plasma ACE-Is. The arterial thrombus weight was reduced in PER and QUIN groups while venous thrombus weight was also reduced after CAP. Tissue andplasma ACE-Is caused the inhibition of platelet adhesion and aggregation. A reduction of fibrin generation, prolongation of prothrombin time (PT), activated partial thromboplastin time (APTT) and shortening of euglobulin clot lysis time (ECLT) were observed after PER and QUIN treatment. In conclusion, given in equipotent hypotensive doses, Tissue ACE-Is exerted more pronounced antithrombotic effect than plasma ACE-Is in experimental thrombosis. The differences between Tissue and plasma ACE-Is in terms of their more pronounced inhibition of experimental thrombosis may be related to the intensified activation of fibrinolysis and inhibition of coagulation.

Ograniczanie wyników

2 Journal of Physiology and Pharmacology

2 Buczko W.

2 Chabielska E.

2 Domaniewski T.

2 Kramkowski K.

2 Mogielnicki A.

1 Kaminska M.

1 Karp A.

1 Malinowska-Zaprzalka M.

1 Opadczuk A.

1 Stankiewicz A.

1 Wojewodzka-Zelazniakowicz M.

1 2006

1 2005

Wyniki wyszukiwania

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

Antithrombotic effect of tissue and plasma type angiotensin converting enzyme inhibitors in experimental thrombosis in rats