Mechanism and modification of bradykinin-induced coronary vasodilation.
AUTOR(ES)
Needleman, P
RESUMO
In isolated perfused rabbit hearts, bradykinin produced a concentration-dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin-E-like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ-20881) markedly enhanced both the coronary vasodilation and release of prostaglandin-E-like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=432693Documentos Relacionados
- Bradykinin-induced contractions of bovine mesenteric lymphatics.
- Autoregulation of bradykinin receptors and bradykinin-induced prostacyclin formation in human fibroblasts.
- Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.
- Bradykinin-induced changes in phosphatidyl inositol turnover in cultured rabbit papillary collecting tubule cells.
- Reduction of the bradykinin-induced activation of feline group III and IV muscle receptors by acetylsalicylic acid.
