Effects of bradykinin on venous capacitance in health and treated chronic heart failure.
Résumé
We investigated the effects of basal and intra-arterial infusion of bradykinin on unstressed forearm vascular volume (a measure of venous tone) and blood flow in health (G1, n=20) and in chronic heart failure patients treated with angiotensin converting enzyme (ACE) inhibitors (G2, n=16) and angiotensin receptor blockers (ARB) (G3, n=14). We used radionuclide plethysmography to examine the effects of bradykinin and of the bradykinin antagonists B9340 (B1/B2 antagonist) and HOE140 (B2 antagonist). Bradykinin infusion increased unstressed forearm vascular volume in a similar dose dependent manner in G1 and G3 (G1 maximum 12.3±2.1%; p<0.001 vs baseline, G3 maximum 9.3±3.3%; p<0.05 vs baseline, p=NS for difference) but the increase in unstressed volume in G2 was higher (maximum 28.8±7.8%; p<0.001 vs baseline; p<0.05 for the difference between groups). In contrast, while the increase in blood flow in G1 (maximum 362±9%; p<0.001) and in G2 (maximum 376±12%; p<0.001) was similar (p=NS for the difference between groups), the increase in G3 was less (maximum 335±7%; p<0.001; p <0.05 for the difference between groups). Infusion of each receptor antagonist alone similarly reduced basal unstressed volume and blood flow in G2 but not in G1 or G3. In conclusion, bradykinin does not contribute to basal venous tone in health, but in ACE inhibitor-treated chronic heart failure it does. In ARB-treated heart failure venous responses to bradykinin are preserved but arterial responses reduced compared with healthy controls. Bradykinin mediated vascular responses in both health and heart failure are mediated by the B2 rather than the B1 receptor.
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