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Effects of bradykinin on venous capacitance in health and treated chronic heart failure

journal contribution
posted on 2023-05-17, 02:38 authored by Gunaruwan, P, Maher, A, Williams, L, James SharmanJames Sharman, Schmitt, M, Campbell, R, Frenneaux, M
In the present study, 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 healthy volunteers (n=20) and in chronic heart failure patients treated with ACEIs [ACE (angiotensin-converting enzyme) inhibitors] (n=16) and ARBs (angiotensin receptor blockers) (n=14). We used radionuclide plethysmography to examine the effects of bradykinin and of the bradykinin antagonists B9340 [B1 (type 1)/B2 (type 2) receptor antagonist] and HOE140 (B2 antagonist). Bradykinin infusion increased unstressed forearm vascular volume in a similar dose-dependent manner in healthy volunteers and ARB-treated CHF patients (healthy volunteers maximum 12.3±2.1%, P<0.001 compared with baseline; ARB-treated CHF patients maximum 9.3±3.3%, P<0.05 compared with baseline; P=not significant for difference between groups), but the increase in unstressed volume in ACEI-treated CHF patients was higher (maximum 28.8±7.8%, P<0.001 compared with baseline; P<0.05 for the difference between groups). In contrast, while the increase in blood flow in healthy volunteers (maximum 362±9%, P<0.001) and in ACEI-treated CHF patients (maximum 376±12 %, P<0.001) was similar (P=not significant for the difference between groups), the increase in ARB-treated CHF patients 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 ACEI-treated CHF patients, but not in healthy volunteers or ARB-treated CHF patients. In conclusion, bradykinin does not contribute to basal venous tone in health, but in ACEI-treated chronic heart failure it does. In ARB-treated heart failure, venous responses to bradykinin are preserved but arterial responses are 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.

History

Publication title

Clinical Science

Volume

116

Issue

5-6

Pagination

443-450

ISSN

0143-5221

Department/School

Menzies Institute for Medical Research

Publisher

Portland Press

Place of publication

59 Portland Place, London, England, W1N 3Aj

Repository Status

  • Restricted

Socio-economic Objectives

Clinical health not elsewhere classified

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