Effect of Bradykinin on Arteries and Veins in Systemic and Pulmonary Circulation

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Abstract
Summary: Bradykinin is a potent vasodilating and natriuretic peptide, which is potentiated by angiotensin-converting enzyme (ACE) inhibitors. In our investigations we studied the effect of bradykinin on systemic and pulmonary circulation as well as on dorsal hand vein tone. The effects of bradykinin on systemic and pulmonary circulation were tested by injection of bradykinin into the right atrium. Parameters were determined for blood pressure, cardiac output, ECG and mean pressure in pulmonary artery. Heart rate, total peripheral resistance, pulmonary vascular resistance, and pulmonary arteriolar resistance were calculated by these measured parameters. The data raised in our investigations showed clearly that bradykinin reduced blood pressure by reducing total peripheral vascular resistance in a dose-dependent manner. In pulmonary circulation bradykinin develops a direct effect. All circulatory actions of bradykinin are not mediated by prostaglandins, since inhibition of prostaglandin synthesis by indomethacin (100–150 mg) was without any effect. ACE inhibition by ramipril (5 mg) or captopril (50 mg) potentiated all effects of bradykinin about 20- to 50-fold, whereas it decreased angiotensin I effects only about four- to fivefold. These results suggest, that endogenous kinins, if they will be similarly potentiated by ACE inhibition like the exogenous bradykinin in our experiments, might play an important role in the blood pressure lowering effect of ACE inhibitors. Dorsal hand vein tone was reduced by bradykinin too, indicating that kinins can lower cardiac preload by increasing venous blood pooling.

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