Cardiovascular Actions and Tissue-Converting Enzyme Inhibitory Effects of Chronic Enalapril and Trandolapril Treatment of Spontaneously Hypertensive Rats

Chevillard, Claude; Brown, Neil L.; Jouquey, Simone; Mathieu, M; Laliberté, François; Hamon, Gilles

doi:10.1097/00005344-198908000-00017

Cited by 23 publications

(10 citation statements)

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“…19 Recently, Linz and coworkers 20 demonstrated that a nonantihypertensive low dose of the ACE-inhibitor ramipril determines the same complete regression of cardiac hypertrophy as seen in a group receiving the antihypertensive dose of ACE inhibitor. In hypertensive rats, Chevillard et al 21 observed that 10 mg/kg of enalapril (i.e., the same drug dose we used) reduced but did not normalize the arterial pressure and simultaneously caused a marked inhibition of myocardial converting enzyme activity.…”

Section: Discussionmentioning

confidence: 90%

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

et al. 1991

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To evaluate the effects of hypertension on cardiac hypertrophy, on myocardial structure, and on ventricular arrhythmias, 27 3-month-old spontaneously hypertensive rats were treated with enalapril (10 ing/kg) daily for 11 months and compared with 26 untreated control rats. Systolic arterial pressure was significantly decreased in treated rats, and at the end of the experiment, it was 199±3 mm Hg (treated) versus 237±3 mm Hg (controls) (p<0.001). At this time, spontaneous arrhythmias and induced arrhythmias either by programmed electrical stimulation (train of stimuli +1 or 2 extrastimuli) or by trains of eight stimuli at decreasing coupling intervals were observed in isolated heart preparations.

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Section: Discussionmentioning

confidence: 90%

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

et al. 1991

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“…It has been suggested that tissue ACE inhibition better describes the pattern of this latter response than the inhibition of ACE in plasma (Cohen & Kurz, 1982;Chevillard et al, 1989;Kamei et al, 1989).…”

Section: Resultsmentioning

confidence: 99%

Transpulmonary pharmacokinetics of an ACE inhibitor (perindoprilat) in man.

Lees

Gemmill

et al. 1991

Brit J Clinical Pharma

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1. The transpulmonary pharmacokinetics of the intravenous diacid ACE inhibitor perindoprilat were studied in 10 male patients undergoing diagnostic cardiac catheterisation for the management of ischaemic heart disease. 2. Following successful completion of diagnostic cardiac catheterisation and ventriculography, subjects received a low dose (1 mg) constant rate infusion of perindoprilat over 20 min with co‐ infusion of the intravenous marker dye indocyanine green (0.5 mg kg‐1). Simultaneous transpulmonary blood sampling was conducted for 1 h and subsequent peripheral venous blood samples were collected for 20 h. 3. No acute changes in blood pressure or heart rate were noted despite rapid and marked inhibition of central circulation plasma ACE activity persisting in peripheral venous blood for 20 h. A delayed rise in plasma renin activity was noted. 4. Transpulmonary passage during early accumulation of the drug was seen to incorporate an early delay. Concurrent ICG measurements suggested that this was entirely due to circulatory delay and not to binding of the drug. Thus, despite the suggested high concentration of tissue ACE activity in the pulmonary circulation, transpulmonary passage of perindoprilat was not measurably influenced by binding at this site under the conditions studied.

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“…Comparison between agents is again complicated by variable potency. Even so, different patterns of inhibition in renal cortical ACE have been demonstrated between agents (Chevillard et al, 1989).…”

Section: Renal and Ras And Ace Activitymentioning

confidence: 99%

Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs.

Lees

Reid

1991

Brit J Clinical Pharma

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1. There is a body of circumstantial and direct evidence supporting the existence and functional importance of a tissue based RAS at a variety of sites. 2. The relation between circulatory and tissue based systems is complex. The relative importance of the two in determining haemodynamic effects is unknown. 3. Despite the wide range of ACE inhibitors already available, it remains unclear whether there are genuine differences related to tissue specificity. 4. Pathological states such as chronic cardiac failure need to be explored with regard to the contribution of tissue based ACE activities in generating acute and chronic haemodynamic responses to ACE inhibitors. 5. The role of tissue vs plasma ACE activity may be clarified by study of the relation between drug concentration and haemodynamic effect, provided that the temporal dissociation is examined and linked to circulating and tissue based changes in ACE activity, angiotensin peptides and sympathetic hormones.

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Cardiovascular Actions and Tissue-Converting Enzyme Inhibitory Effects of Chronic Enalapril and Trandolapril Treatment of Spontaneously Hypertensive Rats

Cited by 23 publications

References 0 publications

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats.

Transpulmonary pharmacokinetics of an ACE inhibitor (perindoprilat) in man.

Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs.

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