Open AccessEffects of arachidonic acid and bradykinin on the coronary flow, release of PGI2 and cardiac functions in the perfused guinea-pig heart.
Author(s) -
Zenichi Terashita,
Hiroshi Fukui,
Kohei Nishikawa,
Minoru Hirata,
Shintarō Kikuchi
Publication year - 1982
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.32.351
Subject(s) - bradykinin , prostacyclin , coronary vasodilator , chronotropic , vasodilation , medicine , arachidonic acid , chemistry , prostaglandin , guinea pig , coronary perfusion pressure , cardiology , endocrinology , heart rate , blood pressure , anesthesia , biochemistry , receptor , cardiopulmonary resuscitation , resuscitation , enzyme
The contribution of prostacyclin (PGI2) to the coronary vasodilating action of arachidonic acid (AA) and bradykinin (BK) was examined in isolated perfused guinea-pig hearts. The injection of Aa (100 to 1,000 ng) and BK (1 to 100 ng) into the heart resulted in a dose-dependent increase in the total amount of coronary flow and a release of 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2. Both AA and BK showed weak positive chronotropic effects. In addition, higher doses (300 and 1,000 ng) of AA caused a transient reduction in the coronary flow rate, left ventricular systolic pressure, and left ventricular dp/dt. The changes in coronary flow, release of PGI2, and all cardiodynamic parameters induced by AA were abolished by pretreatment of the preparation with diclofenac-Na. On the other hand, the BK-induced increase in coronary flow rate was only partially reduced by diclofenac-Na when the release of 6-keto-prostaglandin F1alpha was completely inhibited. It is concluded that in isolated perfused guinea-pig hearts, BK has both PGI2-independent and PGI-2-dependent coronary vasodilating actions; the latter action is less than 25%, and the coronary vasodilating action of AA is mainly mediated via PGI2.