Effects of Captopril on Atherosclerosis in Cynomolgus Monkeys

Åberg, Gunnar; Ferrer, Patricia

doi:10.1097/00005344-199000005-00010

Cited by 180 publications

(43 citation statements)

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“…Chobanion et al [34] showed that captopril decreased both the amount of aortic atherosclerosis and the cellularity of the atherosclerotic lesion in the Watanabe heritable hyperlipidaemic rabbit. Similar results were obtained by Abery and Ferrer in the cholesterol-fed cynomolgns monkey [35]. However, in both these experiments the doses of captopril were 75-to 300-fold those used in a clinical situation.…”

Section: Ace I and Atherosclerosissupporting

confidence: 88%

Angiotensin-converting enzyme inhibitors and coronary artery disease

Sayer

1996

Cardiovasc Drug Ther

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The renin-angiotensin system and angiotensin converting enzyme (ACE) are increasingly being implicated in the pathogenesis of coronary artery disease and its sequelae. Genetic studies of ACE gene polymorphism hint at an association between the ACE genotype and atherosclerosis. Animal studies have demonstrated the potential beneficial effects of ACE inhibition at a variety of sites, including improvement of endothelial function, inhibition of platelet aggregation, reduction of atherosclerosis, and inhibition of myointimal proliferation. Although these have not all been validated in human studies, the reduction of ischemic events in studies of ACE inhibition in left ventricular dysfunction cannot be explained solely by improved hemodynamics, and it is possible that actions on the endothelium, the atherosclerotic process, and platelets are at least in part responsible. The results of studies in humans looking more directly at the influence of ACE inhibitors on atherosclerosis and ischemic heart disease are awaited.

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Section: Ace I and Atherosclerosissupporting

confidence: 88%

Angiotensin-converting enzyme inhibitors and coronary artery disease

Sayer

1996

Cardiovasc Drug Ther

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“…Lesions showed less cellularity and cholesterol content, and an increase in extracellular matrix. Others have also shown results consistent with an antiatherogenic effect in the cholesterol-fed cynomolgus monkey [11] and the minipig [12]. Antimigratory effects on smooth muscle cells and neutrophils have also been shown [13].…”

mentioning

confidence: 74%

Emerging concepts: Angiotensin-converting enzyme inhibition in coronary artery disease

Mancini

1996

Cardiovasc Drug Ther

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Angiotensin-converting enzyme (ACE) inhibitors have played a highly beneficial role in the therapy of hypertension and congestive heart failure. Detailed analysis of some of the heart failure trials in patients with these diseases has uncovered unexpected benefits in the prevention of cardiovascular events. Paralleling these observations are the rapidly accruing basic studies describing important molecular and cellular effects of these agents. For example, ACE inhibition will prevent stimulation of smooth muscle cell angiotensin II receptors, thereby blocking both contractile and proliferative actions. In addition, ACE inhibition of kininase II inhibits the breakdown of bradykinin. Bradykinin is a direct stimulant of nitric oxide release from the intact endothelial cell. Thus, at the cellular level ACE inhibition shifts the balance of ongoing mechanisms in favor of those promoting vasodilatory, antiaggregatory, antithrombotic, and antiproliferative effects. These effects underlie the potential benefits of ACE inhibition in the therapy of coronary artery disease and atherosclerosis.

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“…Several studies in animal models have demonstrated that ACE inhibitors decrease the formation of atherosclerotic lesions through antiproliferative and antimigratory effects [13,14]. ACE inhibitors improve endothelial function in animal models of atherosclerosis [15].…”

Section: Discussionmentioning

confidence: 99%