Combined angiotensin-converting enzyme inhibition and adrenomedullin in an ovine model of heart failure

2002 ◽  
Vol 102 (6) ◽  
pp. 653-660 ◽  
Author(s):  
Miriam T. RADEMAKER ◽  
Chris J. CHARLES ◽  
Garth J.S. COOPER ◽  
David H. COY ◽  
Eric A. ESPINER ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Converting Enzyme ◽  
Creatinine Clearance ◽  
Ace Inhibitor ◽  
Ace Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Creatinine Excretion

Advances in the treatment of heart failure may require manipulation of neurohumoral responses to cardiac impairment in addition to the established strategy of angiotensin-converting enzyme (ACE) inhibition. Importantly, since new treatments are likely to be used in conjunction with ACE inhibition therapy, the effects of the combination of agents need to be assessed. Adrenomedullin (ADM) is a peptide with potent vasodilator and natriuretic actions. ADM and an ACE inhibitor (captopril) were administered for 3h both separately and together in eight sheep with heart failure. Both ADM and captopril alone reduced arterial pressure, left atrial pressure (greater with captopril) and peripheral resistance, and increased cardiac output (greater with ADM). Compared with either treatment separately, combined ADM+captopril produced directionally similar but significantly greater changes in all haemodynamic variables (particularly falls in blood pressure). ADM increased renal sodium and creatinine excretion and creatinine clearance, and maintained urine output. Captopril and ADM+captopril reduced creatinine excretion and creatinine clearance, while urine volume and sodium excretion were not significantly altered. Plasma renin activity rose with all active treatments, whereas angiotensin II levels rose during ADM, but fell during captopril and ADM+captopril. Aldosterone was reduced by all active treatments. ADM+captopril reduced plasma noradrenaline (norepinephrine). In conclusion, short-term co-treatment with ADM and an ACE inhibitor produced significantly greater decreases in ventricular filling pressures and cardiac afterload, and increases in cardiac output, compared with either treatment alone. Despite the greater falls in blood pressure (and presumably renal perfusion pressure), renal function was maintained at a level similar to that observed with captopril alone.

scholarly journals Angiotensin Converting Enzyme Inhibition Activity of Fennel and Coriander Oils from India

2013 ◽  
Vol 8 (5) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Sushil Kumar Chaudhary ◽  
Niladri Maity ◽  
Neelesh Kumar Nema ◽  
Santanu Bhadra ◽  
Bishnu Pada Saha ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitor ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Ace Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Foeniculum Vulgare ◽  
Converting Enzyme Inhibition ◽  
Dpph Radical Scavenging

Foeniculum vulgare Mill and Coriandrum sativum L. are very popular spices in Indian kitchens. The present study was an attempt to evaluate the angiotensin converting enzyme (ACE) inhibition and antioxidant activity of the standardized oils of F. vulgare and C. sativum by an UV method using hippuryl-L-histidyl-L-leucine (HHL) as substrate. Standardization of the oils and identification of the chemical-markers (linalool and anethole) present in them was performed through HPLC and GC-MS. Coriander oil showed the higher ACE inhibition with an IC50 value of 34.8 ± 2.3 μg/mL, than fennel oil with an IC50 value of 40.7 ± 3.5 μg/mL. Both oils showed strong DPPH radical scavenging activity. This finding suggests that coriander and fennel oils can be potential leads for the management of hypertension as an ACE inhibitor.

Chronic angiotensin-converting-enzyme inhibition improves cardiac output and fluid balance during heart failure

1993 ◽  
Vol 264 (2) ◽  
pp. R414-R422 ◽  
Author(s):  
M. W. Brands ◽  
M. Alonso-Galicia ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
D. A. Hildebrandt ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Water Balance ◽  
Angiotensin Converting Enzyme ◽  
Cardiac Function ◽  
Decompensated Heart Failure ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Rate Of Increase ◽  
Sodium And Water Balance

The purpose of this study was to examine the sequential changes in renal and cardiovascular function produced by chronic Benazepril administration at different stages of heart failure in dogs. Heart failure was produced by rapid ventricular pacing in five dogs with a normally functioning renin-angiotensin system (angiotensin normal, AN) and six dogs chronically administered the angiotensin-converting-enzyme inhibitor (ACEI) Benazepril. After 7 days of pacing, cardiac output was significantly higher and total peripheral resistance (TPR) lower in the ACEI compared with the AN dogs. Cumulative sodium and water balance increased significantly in both groups, but after 7 days of pacing there were no significant differences between groups. However, the rate of increase in sodium and water balance was significantly less in the ACEI group. Effective renal plasma flow decreased in the AN and ACEI groups during pacing, but there were no between-group differences, and no significant changes in glomerular filtration rate (GFR) occurred in either group. In the AN dogs, pacing was continued for 7-21 days until the onset of decompensated heart failure. Urinary sodium excretion increased on the first day of ACEI infusion during this stage but returned to pre-ACEI levels during the next 2-3 days. No significant improvement in cardiac output was measured during ACEI in decompensated heart failure. These data suggest that chronic ACEI administration can improve renal and cardiac function in early heart failure without impairing GFR but is less chronic ACEI administration can improve renal and cardiac function in early heart failure without impairing GFR but is less effective in later, decompensated stages.

Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane

1999 ◽  
Vol 96 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Marco GUAZZI ◽  
Piergiuseppe AGOSTONI
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition ◽  
Group 2 ◽  
Alveolar Capillary ◽  
Group 1

Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLco). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLco. Angiotensin-converting enzyme inhibition improves DLco in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLco is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 ;h and 1 and 2 months after starting enalapril treatment (10 ;mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 ;mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 ;h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 ;h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLco despite a decrease in VC. In group 2 patients, nitrates failed to improve DLco and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.

Effect of angiotensin-converting-enzyme inhibition on bradykinin metabolism by vascular endothelial cells

1993 ◽  
Vol 264 (5) ◽  
pp. H1493-H1497 ◽  
Author(s):  
M. Grafe ◽  
C. Bossaller ◽  
K. Graf ◽  
W. Auch-Schwelk ◽  
C. R. Baumgarten ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Vascular Endothelial Cells ◽  
Ace Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Dependent Manner ◽  
Converting Enzyme ◽  
Concentration Dependent Manner ◽  
Cell Monolayers ◽  
Converting Enzyme Inhibition

The degradation of bradykinin by angiotensin-converting-enzyme (ACE) activity in cultured human endothelial cells was studied by direct measurement of bradykinin and by its effect on the release of endothelium-derived relaxing factors. The half-life of exogenous bradykinin (10,000 pg/ml) was calculated from the decay of the bradykinin concentration as 46 +/- 2 min in cell monolayers, 133 +/- 15 min in conditioned medium, and 24 +/- 2 min in homogenates. Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril. Bradykinin-degrading activity was released into the culture medium containing one-fourth of the bradykinin-degrading activity found in the presence of cell monolayers. In cell homogenates higher unspecific bradykinin-degrading activities were present. The functional consequence of bradykinin degradation was demonstrated by the potentiating effect of ramiprilat on the generation of endothelium-derived relaxing factors nitric oxide and prostacyclin from endothelial cells. The study supports the concept of increased vasodilatory effects of bradykinin during ACE inhibition.

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