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Bradykinin infusion in chronic cardiac failure and the effects of captopril
S M Maguire1, D McAuley, C McGurk
1Department of Medicine, Royal Victoria Hospital, BT12 6BA, Belfast, UK.
Insights
Bradykinin (BK) causes vasodilation in patients with chronic cardiac failure (CCF) and controls, with no significant difference between groups. This response is partly nitric oxide (NO)-dependent but unaffected by ACE inhibitors.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Patients with chronic cardiac failure (CCF) exhibit altered vascular responses.
- The role of bradykinin (BK) in CCF vascular function is not well understood, despite its proposed involvement in ACE inhibitor effects.
Purpose of the Study:
- To investigate the direct vasodilatory effects of bradykinin (BK) in patients with chronic cardiac failure (CCF).
- To compare BK responses in CCF patients versus healthy controls.
- To assess the involvement of nitric oxide (NO) and the impact of ACE inhibition on BK-induced vasodilation in CCF.
Main Methods:
- Forearm blood flow (FBF) was measured using venous occlusion plethysmography in 10 CCF patients and 10 controls.
- Bradykinin (BK) was infused at varying doses (10, 30, 100 pmol min(-1)).
- Responses were re-evaluated with co-administration of N(G)-monomethyl L-arginine (L-NMMA) and after captopril administration.
Main Results:
- Bradykinin (BK) induced dose-dependent vasodilation in both CCF patients and controls, with no significant difference between groups (P=0.77).
- The vasodilator response to BK was reduced by L-NMMA in both groups, indicating partial NO-dependency.
- The vasodilator response to BK remained unchanged after captopril administration in CCF patients (P=0.53).
Conclusions:
- Bradykinin (BK) produces comparable dose-dependent vasodilation in patients with chronic cardiac failure (CCF) and healthy individuals.
- The BK-induced vasodilation is partially nitric oxide (NO)-dependent, as evidenced by antagonism with L-NMMA.
- ACE inhibition with captopril did not alter the vasodilatory response to bradykinin (BK) in CCF patients.
Background:
Patients with chronic cardiac failure (CCF) have abnormal vascular responses. Bradykinin (BK) is thought to contribute to the vasodilator effects of ACE inhibitors, but the effect of BK itself in patients with CCF has not been examined.
Methods:
We studied the responses to infused BK at 10, 30 and 100 pmol min(-1) in patients with CCF (n=10) and controls (n=10). The slope of the dose-response curve was used for comparisons between the groups. Forearm blood flow (FBF) was measured by venous occlusion plethysmography.
Results:
Following BK, vasodilatation was observed in both groups as the slopes were positive in all, but the difference between the groups was not significant (P=0.77). The study was repeated with the co-administration of 4 micromol min(-1) of N(G)-monomethyl L-arginine (L-NMMA). The vasodilator response to BK was reduced in both groups, and the effect was somewhat greater in the patient group (P=0.23). The vasodilator response to the endothelium-independent vasodilator sodium nitroprusside was slightly less in the patient group (P=0.08). The patients only then underwent repeat infusion of BK before and after a single oral dose of captopril 12.5 mg or placebo. Following captopril, the vasodilator response to BK was unchanged when compared to placebo (difference between slopes, P=0.53).
Conclusions:
BK produces dose-dependent vasodilatation in both patients with CCF and controls; there was no difference in the responses, which were antagonised by L-NMMA and therefore in part NO (endothelium)-dependent. The responses were also unchanged after administration of an ACE inhibitor (captopril).
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