Cardiovascular effects of leukotrienes

Leukotrienes are among the most potent lipid mediators of inflammation. Leukotriene B4 is one of the most potent endogenously synthesized chemotactic substances. It is probable that LTB4 plays an important role in the initial phase of the inflammatory reaction. The peptidoleukotrienes LTC4 and LTD4 are potent broncho- and vasoconstrictors. Administration of LTC4 and LTD4 leads to an increase of blood pressure in most species. These effects are sometimes dependent on the liberation of vasoactive prostaglandins. In addition, peptidoleukotrienes enhance vascular permeability rapidly. Peptidoleukotrienes elicit coronary vasoconstriction which is the most likely reason for the negative inotropic effect of these compounds. Recently the synthesis of peptidoleukotrienes has been demonstrated in the heart under experimental conditions. While the kidney shows a relatively mild vasoconstrictor response to leukotrienes, the pulmonary vascular bed generally responds with a brisk increase of resistance. Pathophysiological roles of leukotrienes require further definition. A striking increase in leukotrienes synthesis has been observed following endotoxin shock.