Contrasting patterns of arterial and venous dilatation after intravenous captopril in patients with chronic cardiac failure and their relationship to plasma angiotensin II concentrations

Flapan, A. D.; Shaw, T. R. D.; Edwards, C. R. W.; Davies, Eleanor; Williams, Brent C.

doi:10.1016/0002-8703(92)90411-n

Cited by 5 publications

(7 citation statements)

References 38 publications

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“…It has been widely established that ACE inhibitor therapy has major therapeutic benefits in patients with heart failure, 1,2 which include improvements in morbidity, exercise capacity, and mortality. 1, 3 The administration of ACE inhibitor therapy in these patients causes systemic vasodilatation 4 that has been attributed to the loss of angiotensin II-mediated vasoconstriction. However, it is unknown whether the vasodilatation associated with ACE inhibitor therapy may in part relate to the concomitant blockade of bradykinin degradation.…”

mentioning

confidence: 99%

Bradykinin Contributes to the Vasodilator Effects of Chronic Angiotensin-Converting Enzyme Inhibition in Patients With Heart Failure

et al. 2001

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Background-Bradykinin, an endogenous vasodilator peptide, is metabolized by ACE. The aims of the present study were to determine the doses of B9340, a bradykinin receptor antagonist, that inhibit vasodilatation to exogenous bradykinin and to assess the contribution of bradykinin to the maintenance of basal vascular tone in patients with heart failure receiving chronic ACE inhibitor therapy. Methods and Results-Forearm blood flow was measured using bilateral venous occlusion plethysmography. On three occasions in a double-blind randomized manner, 8 healthy volunteers received intrabrachial infusions of placebo or B9340 (at 4.5 and 13.5 nmol/min). On each occasion, placebo or B9340 was coinfused with bradykinin (30 to 3000 pmol/min) and substance P (4 to 16 pmol/min). B9340 caused no change in basal FBF but produced dose-dependent inhibition of the vasodilatation to bradykinin (PϽ0.001) but not substance P. The effects of bradykinin antagonism were studied in 17 patients with NYHA grade II through IV heart failure maintained on chronic ACE inhibitor therapy. Incremental doses of B9340, but not HOE-140, produced a dose-dependent vasoconstriction (Pϭ0.01). After withdrawal of ACE inhibitor therapy, B9340 produced no significant change in forearm blood flow. After reinstitution of therapy, B9340 again resulted in vasoconstriction (PϽ0.03). Conclusions-B9340 is a potent and selective inhibitor of bradykinin-induced vasodilatation. Bradykinin does not contribute to the maintenance of basal peripheral arteriolar tone in healthy humans or patients with heart failure but contributes to the vasodilatation associated with chronic ACE inhibitor therapy in patients with heart failure via the B 1 receptor.

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confidence: 99%

Bradykinin Contributes to the Vasodilator Effects of Chronic Angiotensin-Converting Enzyme Inhibition in Patients With Heart Failure

et al. 2001

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“…A11 levels were not measured and its effect in our study remains speculative. Although A11 possibly has a direct inotropic effect on the heart (Koch-Weser 1965;Freer et al 1976), and enkephalin supposedly inhibits sympathetic discharge (Araujo & Collier 1978;Horiuchi et al 1989), we could not demonstrate a reduction in cardiac inotropism with captopril using Q S L No effect of A11 on venous capacitance (Flapan et al 1992;Motwani & Struthers 1992) was evident from the preload-sensitive STI, PEP index and PEP/LVET (Buch et al 1980).…”

Section: Discussionmentioning

confidence: 58%

“…Captopril given in cardiac failure causes a reduction in peripheral resistance not entirely related to the drop in A11 (Flapan et al 1992). It is therefore possible that under conditions of high resting sympathetic activity such as cardiac failure, the results could have been different.…”

Section: Discussionmentioning

confidence: 99%

The Influence of Captopril and Naloxone on the Valsalva Manoeuvre and Systolic Time Intervals in Healthy Volunteers

Richter

Sommers

Snyman

1994

Clin Exp Pharma Physio

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1. The aim of the study was to ascertain whether the inhibition of the sympathetic nervous system by angiotensin-converting enzyme (ACE) inhibitors is mediated by endogenous opioids. Naloxone was used to evaluate the effects of the latter on systolic time intervals (STI) and Valsalva manoeuvre-induced blood pressure and heart rate changes. 2. Baseline recordings were done in 12 healthy male volunteers and repeated 2 h after oral administration of 75 mg of captopril and again after naloxone 0.4 mg/kg was administered intravenously over 10 min. 3. After captopril there was a significant reduction in systolic (P < 0.02) and mean blood pressure (P < 0.04) without any changes in heart rate. Furthermore, captopril increased the Valsalva ratio (P < 0.06) but did not influence inotropism as indicated by STI. Naloxone did not influence any of these findings. 4. The changes in the Valsalva ratio after captopril were mediated by an increase in the maximum bradycardia in nine of the 12 subjects. 5. The results indicate that endogenous opioids do not play a role in the putative sympatholytic effect of ACE inhibition.

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“…Therapy with ACE inhibition has known benefits in patients with heart failure including improvements in functional capacity, morbidity, and mortality 25–28. The administration of ACE inhibitor therapy in these patients causes systemic vasodilation, attributable to the loss of angiotensin II-mediated vasoconstriction 29. Recently, however, it has been suggested that the vasodilatory properties of bradykinin also contribute to the ACE inhibitor-induced vasodilation in both the radial and coronary arteries 13,30.…”

Section: Discussionmentioning

confidence: 99%

Gene Variant of the Bradykinin B2 Receptor Influences Pulmonary Arterial Pressures in Heart Failure Patients

Olson¹,

Frantz²,

Turner³

et al. 2009

Clinical medicine. Circulatory, respiratory and pulmonary medic

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Contrasting patterns of arterial and venous dilatation after intravenous captopril in patients with chronic cardiac failure and their relationship to plasma angiotensin II concentrations

Cited by 5 publications

References 38 publications

Bradykinin Contributes to the Vasodilator Effects of Chronic Angiotensin-Converting Enzyme Inhibition in Patients With Heart Failure

Bradykinin Contributes to the Vasodilator Effects of Chronic Angiotensin-Converting Enzyme Inhibition in Patients With Heart Failure

The Influence of Captopril and Naloxone on the Valsalva Manoeuvre and Systolic Time Intervals in Healthy Volunteers

Gene Variant of the Bradykinin B2 Receptor Influences Pulmonary Arterial Pressures in Heart Failure Patients

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