Angiotensin II contributes to arterial compliance in congestive heart failure

2002 ◽  
Vol 283 (4) ◽  
pp. H1424-H1429 ◽  
Author(s):  
Silvia G. Lage ◽  
Liliane Kopel ◽  
Caio C. J. Medeiros ◽  
Ricardo T. Carvalho ◽  
Mark A. Creager
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Carotid Artery ◽  
Angiotensin Converting Enzyme ◽  
Arterial Compliance ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Favorable Effect ◽  
Converting Enzyme ◽  
Patients With Heart Failure

Arterial compliance is determined by structural factors, such as collagen and elastin, and functional factors, such as vasoactive neurohormones. To determine whether angiotensin II contributes to decreased arterial compliance in patients with heart failure, this study tested the hypothesis that administration of an angiotensin-converting enzyme inhibitor improves arterial compliance. Arterial compliance and stiffness were determined by measuring carotid artery diameter, using high-resolution duplex ultrasonography, and blood pressure in 23 patients with heart failure secondary to idiopathic dilated cardiomyopathy. Measurements were made before and after intravenous administration of enalaprilat (1 mg) or vehicle. Arterial compliance was inversely related to both baseline plasma angiotensin II ( r = −0.52; P = 0.015) and angiotensin-converting enzyme concentrations ( r = −0.45; P = 0.041). During isobaric conditions, enalaprilat increased carotid artery compliance from 3.0 ± 0.4 to 5.0 ± 0.4 × 10−10N−1· m4( P = 0.001) and decreased the carotid artery stiffness index from 17.5 ± 1.8 to 10.1 ± 0.6 units ( P = 0.001), whereas the vehicle had no effect. Thus angiotensin II is associated with reduced carotid arterial compliance in patients with congestive heart failure, and angiotensin-converting enzyme inhibition improves arterial elastic properties. This favorable effect on the pulsatile component of afterload may contribute to the improvement in left ventricular performance that occurs in patients with heart failure treated with angiotensin-converting enzyme inhibitors.

scholarly journals Acute effects of angiotensin-converting enzyme inhibition versus angiotensin II receptor blockade on cardiac sympathetic activity in patients with heart failure

2017 ◽  
Vol 313 (4) ◽  
pp. R410-R417 ◽  
Author(s):  
Eduardo R. Azevedo ◽  
Susanna Mak ◽  
John S. Floras ◽  
John D. Parker
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Sympathetic Activity ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Acute Effects ◽  
Beneficial Effects ◽  
Patients With Heart Failure ◽  
Total Body

The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (ANG II) receptor antagonists in patients with heart failure secondary to reduced ejection fraction (HFrEF) are felt to result from prevention of the adverse effects of ANG II on systemic afterload and renal homeostasis. However, ANG II can activate the sympathetic nervous system, and part of the beneficial effects of ACE inhibitors and ANG II antagonists may result from their ability to inhibit such activation. We examined the acute effects of the ACE inhibitor captopril (25 mg, n = 9) and the ANG II receptor antagonist losartan (50 mg, n = 10) on hemodynamics as well as total body and cardiac norepinephrine spillover in patients with chronic HFrEF. Hemodynamic and neurochemical measurements were made at baseline and at 1, 2, and 4 h after oral dosing. Administration of both drugs caused significant reductions in systemic arterial, cardiac filling, and pulmonary artery pressures ( P < 0.05 vs. baseline). There was no significant difference in the magnitude of those hemodynamic effects. Plasma concentrations of ANG II were significantly decreased by captopril and increased by losartan ( P < 0.05 vs. baseline for both). Total body sympathetic activity increased in response to both captopril and losartan ( P < 0.05 vs. baseline for both); however, there was no change in cardiac sympathetic activity in response to either drug. The results of the present study do not support the hypothesis that the acute inhibition of the renin-angiotensin system has sympathoinhibitory effects in patients with chronic HFrEF.

Effect of angiotensin-converting enzyme inhibition on plasma brain natriuretic peptide levels in patients with heart failure

1992 ◽  
Vol 83 (2) ◽  
pp. 143-147 ◽  
Author(s):  
Chim C. Lang ◽  
Joseph G. Motwani ◽  
Abdul R. Rahman ◽  
Wendy J. Coutie ◽  
Allan D. Struthers
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Congestive Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Patients With Heart Failure

1. The aim of this study was to examine the effect of captopril, an angiotensin-converting enzyme inhibitor, on plasma levels of human brain natriuretic peptide-like immunoreactivity (hBNP-li) in patients with congestive heart failure. 2. Six male patients (aged 52–74 years) with mild to moderate congestive heart failure were studied on two occasions in the semi-recumbent position. After a 30 min rest, patients were randomized to receive oral tablets of either captopril (6.25 mg followed by 25 mg 2 h later) or placebo in a single-blind manner. Plasma hBNP-li, atrial natriuretic peptide-like immunoreactivity (ANP-li) and angiotensin II-like immunoreactivity (ANG II-li) levels and blood pressure were measured. 3. Baseline plasma hBNP-li and ANP-li levels in these patients with mild to moderate congestive heart failure were 13.5 ± 3.2 pmol/l and 50.9 ± 11.8 pmol/l, respectively. In 11 healthy male subjects aged 20–23 years, the peripheral plasma hBNP-li and ANP-li levels were 1.3 ± 0.2 pmol/l and 5.6 ± 1.7 pmol/l, respectively. In all patients, captopril decreased the plasma ANG II-li level (from 24.3 ± 8.1 to 6.6 ± 3.2 pmol/l, P<0.05) and mean arterial blood pressure (from 92 ± 3 to 80 ± 3 mmHg, P<0.05). Compared with placebo, captopril treatment was associated with significant reductions in plasma hBNP-li (from 14.3 ± 3.0 to 12.8 ± 2.1 pmol/l, P<0.05) and in plasma ANP-li (from 53.9 ± 1.11 to 36.8 ± 7.6 pmol/l, P<0.05) levels. 4. Our results show that in patients with heart failure, acute inhibition of angiotensin-converting enzyme with captopril results in falls in both plasma hBNP-li (10% fall) and ANP-li (32% fall) levels. Our results do not support a major role for angiotensin-converting enzyme in the metabolism of human brain natriuretic peptide in heart failure, although a minor role cannot be excluded since the fall in the plasma ANP-li level was greater than the fall in the plasma hBNP-li level. However, the fall in the plasma hBNP-li level is most probably related to the changes induced in intra-cardiac volume/pressure by the angiotensin-converting enzyme inhibitor.

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