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Role of ACE Inhibitors in Hypertension Complicated by Vascular Disease S 37

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Role of ACE Inhibitors in Hypertension Complicated by Vascular Disease S 37 Br Heart Jf (Supplement) 1994; 72: 33-37 S 33 Role of ACE inhibitors in hypertension Br Heart J: first published as 10.1136/hrt.72.3_Suppl.S33 on 1 September 1994. Downloaded from complicated by vascular disease Gordon T McInnes Hypertension is an important risk factor for Locally produced angiotensin II may exert a vascular disease. Therefore, it is not surprising significant effect on vascular tone directly by that many patients with hypertension have contracting smooth muscle and indirectly by widespread atherosclerotic disease. Treatment releasing catecholamines from surrounding with conventional antihypertensive drugs can nerve endings. Direct clinical evidence be problematic in such patients. In this article suggests that tissue actions may influence I consider the use of angiotensin converting regional blood flow. Thus, enalapril, at a dose enzyme (ACE) inhibitors in managing hyper- which did not induce significant humoral or tension complicated by vascular disease, pay- systemic haemodynamic effects, reduced left ing particular attention to cerebrovascular ventricular inotropic state and increased disease and peripheral vascular disease affect- coronary blood flow when infused into the ing the legs. Coronary artery disease and coronary bed and increased forearm blood atherosclerotic renovascular disease are flow when infused into the forearm.' considered only briefly. Vascular angiotensin II may be a major ACE inhibitors reduce blood pressure in pathological factor in the development of hypertensive patients by decreasing peripheral atherosclerosis (figure), mediating the pro- resistance with little effect on cardiac output liferation of arterial smooth muscle cells by or heart rate. The lack of reflex tachycardia is many mechanisms, including a direct effect on likely to be due to downward resetting of growth factor production and reciprocal sup- baroceptor reflexes, though ACE inhibitor pression of arterial bradykinin concentrations. induced venodilatation or modification of The effects of ACE inhibition on pro- parasympathetic activity may contribute. The gression of atherosclerosis has been reviewed increase in arterial compliance due to ACE recently by Sharpe.2 Early studies showed no inhibition can influence regional haemo- beneficial effect on aortic atherosclerosis in dynamics, with redistribution of blood flow rabbits fed cholesterol, but in more recent in favour of vital organs. ACE inhibitors work captopril was effective in Watenabe rabbits, increase blood flow and decrease vascular which have an inherited tendency to secondary resistance in the regions supplied by the renal, hyperlipidaemia, without affecting serum carotid, and brachial arteries both in healthy cholesterol concentration; total aortic surface subjects and in patients with hypertension. involvement and the cellularity of athero- http://heart.bmj.com/ Unlike some other antihypertensive agents, sclerotic lesions were reduced. In cynomolgus such as P blockers, ACE inhibitors do not monkeys fed cholesterol, low and high doses interfere with the normal haemodynamic of captopril reduced atherosclerotic lesions in responses to stress or exercise while blood carotid arteries by 80% and 95% respectively; pressure reduction is maintained. As a conse- coronary arteries were almost free of athero- quence of these haemodynamic properties, sclerosis after ACE inhibition. Continuous or ACE inhibitors might be particularly suitable treatment with cilazapril captopril prevented on September 30, 2021 by guest. Protected copyright. for the treatment of hypertension complicated neointimal proliferation after carotid endo- by atherosclerosis. thelial denudation injury by balloon catheter- The beneficial haemodynamic effects of isation; this was not primarily due to blood ACE inhibitors in hypertension are mediated pressure reduction as verapamil was ineffec- primarily by inhibition of ACE and the conse- tive. Similar findings have been reported with quent withdrawal of the vasoconstricting action lisinopril and perindopril in various animal of endogenous angiotensin II. Since ACE can models of atherosclerosis. These actions are also affect bradykinin degradation, some of the likely to be due to blockade of angiotensin II vascular actions of some ACE inhibitors might since the same effect has been seen with an be mediated by changes in concentrations of AT1 receptor antagonist.3 Preservation of vasoactive kinins and prostanoids. Although the effects of captopril may depend partly on Hypertension Vascular injury University with other ACE Department of such mechanisms, studies Medicine and inhibitors have failed to show changes in Therapeutics, prostaglandin metabolism. Induction of vascular ACE Gardiner Institute, Animal studies suggest that tissue ACE and Western Infirmary, Glasgow angiotensin II (particularly in the vasculature) G T McInnes may be more important than plasma concen- Increase in local angiotensin 11 Correspondence to: trations in determining the haemodynamic Dr G T McInnes, inhibitors. It is unclear whether University Department of effects of ACE Medicine and Therapeutics, the local effects of ACE inhibitors are entirely Vascular remodelling Gardiner Institute, to inhibition of local II or II as a in the Westem Infirmary, due angiotensin Vascular angiotensin pathological factor Glasgow G1 1 6NT. interference with other peptide systems. development of atherosclerosis. S 34 McInnes Table 1 Possible endothelial function with ACE inhibitors has with decreased sympathetic drive and increased mechanisms of effect of been shown in the aortic segments of rabbits compliance of large vessels. The vasodilating Br Heart J: first published as 10.1136/hrt.72.3_Suppl.S33 on 1 September 1994. Downloaded from ACE inhibitors on atherosclerosis on a long term atherogenic diet,2 possibly action of ACE inhibitors on peripheral vessels through accumulation of bradykinin, which might lead to improved blood flow to the Mechanism enhances release of endothelial derived limbs. Ancillary actions such as inhibition of Reduction in blood pressure relaxing factor and production of cyclic AMP platelet aggregation and thromboxane A2 Reduction in arterial Thus or release after captopril may be particularly permeability and (cAMP). ACE inhibitors may prevent lipoprotein entry retard the development of atherosclerosis. advantageous since hyperaggregability of Inhibition of growth factors: Table 1 lists potential mechanisms. Angiotensin II platelets may contribute to the atherogenic Platelet derived growth process and to formation of mural thrombi factor Fibroblast growth factor and platelet emboli. Epidermal growth factor Peripheral vascular disease In healthy subjects ACE inhibitors have Transforming growth Intermittent is the flow to the factor a claudication primary been reported to increase blood Free radical scavenging symptom of chronic occlusive peripheral arms and legs. Blood flow to skeletal muscle (SH group) and on antioxidant for low density vascular disease of the legs. Like hypertension, and skin is augmented because of an action lipoprotein cholesterol its prevalence increases with age. Its pattern is large arteries and arterioles and because of Anti-inflammatory effects similar to that of angina but it occurs 10 years improved compliance.6 By contrast, other later; 3-20% of subjects over 65 years are studies have indicated no change in limb affected.4 Atheroma is a generalised disease, blood flow with captopril in hypertensive and intermittent claudication might be subjects.7 Peripheral vasodilatation is offset by expected to coexist with coronary artery lowered perfusion pressure and flow is disease and cerebrovascular disease. About unaltered; the normal response to exercise is 50% of sufferers have evidence of myocardial maintained. These effects may not be ischaemia; a smaller proportion have cerebro- accompanied by clear clinical advantages. vascular disease. About 15% have myocardial Herrick et al found no difference between infarction and 5% a stroke within five years. enalapril and atenolol in exercise duration, Only two approaches have been shown to be subjective dyspnoea, or tiredness in hyper- of benefit in improving symptoms: stopping tensive patients.' smoking and regular exercise. Angioplasty or Anecdotal reports suggest that the symp- reconstructive surgery offers good relief of toms of peripheral vascular disease seen with symptoms if there is continuous serious 3 blockers may improve dramatically by handicap for at least one year despite con- switching to treatment with an ACE inhibitor. servative measures; pain at rest; or gangrene. Properly conducted studies of ACE inhibitors Medical treatment of coexistent hypertension, in hypertensive patients with peripheral hyperlipidaemia, and diabetes mellitus may be vascular disease are difficult to find. Uncon- required, but there is no evidence that this trolled observations in 20 patients treated with leads to symptomatic improvement. captopril 50 mg daily for eight weeks indicated The optimal choice of treatment for hyper- improvement in ankle/arm pressure index at tension complicated by peripheral vascular rest and after exercise, in absolute pain free http://heart.bmj.com/ disease is limited by the unwanted effects on interval, and in reduction in blood pressure.9 peripheral vascular resistance and regional Libretti and Catalano also compared captopril haemodynamics of many of the most effective at the same dose with chlorthalidone 25 mg drugs currently available. Antihypertensive daily in 20 hypertensive
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