Key result
Intra-arterial bradykinin infusion increased unstressed forearm vascular volume more in ACEI-treated CHF patients (28.8%) than in healthy volunteers (12.3%) or ARB-treated patients (9.3%) (P<0.05).
Why the study?
Does intra-arterial bradykinin infusion affect venous capacitance and blood flow differently in healthy volunteers compared to chronic heart failure patients treated with ACE inhibitors or ARBs?
Does intra-arterial bradykinin infusion affect venous capacitance and blood flow differently in healthy volunteers compared to chronic heart failure patients treated with ACE inhibitors or ARBs?
Absolute Event Rate: 28.8% vs 12.3%
p-value: p=<0.05
Bradykinin contributes to basal venous tone in ACE-inhibitor treated heart failure patients but not in healthy individuals or ARB-treated patients, with vascular responses mediated primarily by the B2 receptor.
Bradykinin may contribute to basal venous tone only with ACEIs in HF; leaves open clinical relevance and need for outcome studies.
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.
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Gunaruwan et al. (2008) studied Chronic heart failure (n=50). Bradykinin vs. Healthy volunteers and ARB-treated CHF patients was evaluated on Unstressed forearm vascular volume (p=<0.05). Intra-arterial bradykinin infusion increased unstressed forearm vascular volume more in ACEI-treated CHF patients (28.8%) than in healthy volunteers (12.3%) or ARB-treated patients (9.3%) (P<0.05).
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