Autor: Tsunehiro Kawamura, Teruo Kitani, Mitsuro Watada, Yasushi Okajima, Kenhiro Rin, Shunyo Kanayama, Yoshiharu Maeda, Masao Nakagawa, Kichiro Osamura, Hamao Ijichi
Rok vydání: 1983
Předmět:
Zdroj: Blood & Vessel. 14:65-69
ISSN: 1884-2372
0386-9717
DOI: 10.2491/jjsth1970.14.65
Popis: Vasodilator drugs have often been applied clinically to the patients with ischemic heart disease or hypertension, and their antiplatelet activity have been evaluated recently. This paper reports the effects of Hydralazine, Budralazine, Verapamil and Nicardipine, on the platelet aggregation and PGI2 generation from rat aorta.Effects of the drugs on the platelet aggregation in vitro were evaluated by ADP, arachidonic acid (A. A.) and collagen induced aggregation. Effects of drugs on the PGI2 generation from rat aorta in vitro and in vivo were examined by a bioassay system. ADP-induced platelet aggregation was inhibited dose dependently by these drugs at the higher concentrations than 10-4M. A. A. and collagen-induced platelet aggregations were partially inhibited at 10-4M of these drugs, and completely inhibited at the concentration over 2×10-4M. These drugs increased PGI2 generation of rat aorta both in vitro (10-5-10-7M) and in vivo (1mg/Kg).when hydrocortisone, a phospholipase A2 inhibitor, was added to the incubation system of anrta PGI2 activity was not increased even in the presence of Verapamil. However when A. A. was added to this incubation medium, PGI2 generation was recovered and increased with the addition of Verapamil. These results indicate that Verapamil increases the PGI2 generation in the process of A. A. metabolism.In the action of these vasodilators, it was confirmed that the prostaglandins, especially PGI2 and TXA2, were involed. And it is suspected that Ca-antagonist affects the process after liberation of arachidonic acid.
Databáze: OpenAIRE
Externí odkaz: