Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibitors of angiotensin-converting enzyme are used commonly nowadays for the treatment of hypertension and cardiac failure. Over the past two years, shortly after the introduction of this type of drug the occurrence of acute renal failure mainly in elderly patients has been reported. The authors have insisted that strict control of renal function and electrolytes are necessary before and after administration of an ACE inhibitor. Particular caution is needed in patients with severe atherosclerotic disease, especially if bilateral (or unilateral in patients with a single kidney) renal arterial stenosis is present or suspected. Considering these limitations ACE inhibitors remain well tolerated and beneficial cardiovascular drugs.
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PMID:[Converting enzyme inhibitors and acute renal insufficiency--precautions to be taken]. 192 94

Arteriosclerosis is the hallmark of hypertension and of its complications, namely stroke, coronary artery disease and ischaemic renal failure. The earliest morphological change in the arteriosclerotic process is vascular smooth muscle hypertrophy and hyperplasia. Angiotensin II is an important growth factor in vascular smooth muscle cells. The chronic administration of ACE inhibitors will reverse many of the changes of vascular hypertrophy in experimental animal models, and will improve vascular compliance in hypertensive patients. Some differences have been reported between different ACE inhibitors with respect to blood pressure-lowering effect and regression of medial hypertrophy in spontaneously hypertensive rats.
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PMID:Reversal of structural changes in hypertensive arteries--a major prospect for the future. 192 14

ACE inhibition may be useful in several manifestations of ischaemic heart disease, such as heart failure due to ischaemic cardiomyopathy. Recent evidence suggests that these effects may also be present in normotensive patients with ischaemic heart disease without heart failure. Theoretically, converting-enzyme inhibition, through coronary and systemic vasodilating effects and negative inotropic properties, should have a favourable effect on the myocardial oxygen supply/demand ratio and, hence, affect the incidence and severity of myocardial ischaemia. It is doubtful, however, whether these cardiac and extracardiac properties of ACE inhibitors really underlie its potential antiischaemic effects, at least in the average patient with ischaemic heart disease without concomitant heart failure and hypertension. Recent animal and human studies indicate that converting-enzyme inhibitors may modulate myocardial ischaemia by reducing ischaemia-induced circulating neurohumoral activation. It has been shown that, depending on the severity of ischaemia, the circulating renin-angiotensin system may become activated together with an increase in circulating catecholamine levels. ACE inhibition suppresses this neuroendocrine stimulation during ischaemia and modulates subsequent systemic and, presumably, also coronary vasoconstriction. In addition to these effects on circulating neurohormones, ACE inhibition could affect myocardial ischaemia through a number of local actions, e.g. modulation of tissue (cardiac) angiotensin II formation and bradykinin breakdown, stimulation of prostaglandin synthesis and, in the use of sulphydryl compounds, by affecting EDRF formation. Whether ACE inhibitors have clear antiischaemic effects in all clinical conditions is uncertain. Their efficacy to limit exercise-induced ischaemia has been questioned. In contrast, pacing-induced ischaemia in patients at rest is clearly prevented by ACE inhibition. This differential effect may be related to a more pronounced difference in circulating neurohormones during exercise per se. It also suggests that ACE inhibitors may be particularly useful as (additional) antiischaemic therapy in patients with angina at rest, e.g. unstable angina and the acute phase of myocardial infarction.
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PMID:Neurohumoral activation during acute myocardial ischaemia. Effects of ACE inhibition. 197 98

A prospective population study of women in Gothenburg, Sweden, showed an increased risk of developing diabetes in women taking diuretics or beta-blockers as antihypertensive agents compared to other women. The risk seemed to be still higher, if the combination of diuretics and beta-blockers was used. The same observation was made also when the study was confined to hypertensive women indicating that not only the hypertensive state but also the antihypertensive drugs per se may be a risk factor for developing diabetes. This possibility is further strengthened by the fact that, as far as diabetes type II is concerned, the hypertensive state in most cases precedes the development of diabetes, while only few subjects with diabetes type II develop arterial hypertension. We could only study the possible diabetic effect of diuretics and beta-blockers. It must, however, be of great interest to study alpha-blockers, calcium antagonists and ACE inhibitors in the same way. If one or more of these new substances will prove not to be diabetogenic, this will be a very important factor in our choice of first drug in the treatment of arterial hypertension.
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PMID:Incidence of diabetes during antihypertensive treatment. 197 45

NIDDM and hypertension are both characterized by insulin resistance and/or hyperinsulinemia. In IDDM, factors associated with nephropathy produce hypertension. To avoid exacerbation of the metabolic condition, and to prevent further deterioration in glycemic control, treatment of hypertension in the diabetic patient should include the administration of medication with the fewest adverse effects on glucose homeostasis. If diuretics are to be used, it appears that loop diuretics may be preferable to the thiazides or potassium-sparing compounds. Among the remaining classes of antihypertensive drugs, ACE inhibitors may be the agents of choice because of their potential positive effects on insulin sensitivity and renal function, and their lack of severe adverse side-effects.
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PMID:Insulin sensitivity and blood lipids during antihypertensive treatment with special reference to ACE inhibition. 197 44

Overweight and obesity may develop in individuals with genetically determined low resting energy expenditure. Drugs are among the recognised precipitating factors. The obesity promoting impact of beta-blockers is, however, less well known. Resting energy expenditure, and thermogenesis induced by stimuli such as meals, cold and heat exposure, stress and anxiety, have a facultative component mediated by the sympathoadrenal system through catecholamines working on beta-adrenoceptors. Treatment with beta-blockers reduces the facultative thermogenesis by 50-100 kcal/d, which corresponds to the weight gain of 2-5 kg/year reported in clinical trials. Treatment with beta-blockers also results in insulin resistance, which may aggravate existing diabetes and elicit diabetes in predisposed patients. Overweight and obesity are frequently complicated with hypertension and angina pectoris, which are often treated with beta-blockers. Obesity is associated with a defective sympathetic activity, and treatment with beta-blockers may further reduce facultative thermogenesis and promote weight gain. The consequence may be aggravation of hypertension, insulin resistance and other atherogenic factors. The causal therapy of android overweight and obesity complicated with diabetes or hypertension is a sufficient weight loss. If pharmacological treatment is inevitable, combined treatment with diuretics and ACE-inhibitors are most appropriate.
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PMID:[Obesity and diabetes as side-effects of beta-blockers]. 197 28

Hypertension occurs in about 40% of patients with non-insulin-dependent diabetes mellitus (NIDDM) in whom the incidence of coronary heart disease is greatly increased. Disturbances in lipid metabolism may be an important contributory factor. Patterns of lipid change in uncomplicated NIDDM are characterised by a raised serum triglyceride and a reduced high density lipoprotein. It is therefore likely that therapy for hypertension associated with NIDDM may further influence an existing atherogenic lipid profile. Recent studies in diabetic subjects have shown that alpha-blockers are associated with a trend towards improving, while beta-blockers adversely affect, the lipid profile. Calcium antagonists and ACE inhibitors have no adverse effects on the lipid profile.
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PMID:Antihypertensive drugs and the hypertensive diabetic patient. 197 21

The pathophysiological connections between insulin resistance, hypertension and type 2 diabetes are discussed in this review article. Increased blood pressure levels are often found in type 2 diabetic patients long before the diabetes itself is diagnosed. By contrast, in type 1 diabetes hypertension is predominantly the consequence of diabetic glomerulopathy. Non-pharmacological strategies should be favoured in the treatment of hypertension in type 2 diabetic patients before specific pharmacological intervention is started. Antihypertensive treatment with beta-blocking agents and diuretics is criticized by many experts in the field of metabolic disorders, since these drugs induce a deterioration of glycaemic control and lipid metabolism in diabetic patients. Since calcium channel blockers, ACE inhibitors and alpha 1-specific blocking agents have no influence on metabolism, these drugs are recommended for the antihypertensive treatment of diabetic patients. Further studies should be undertaken to clarify, whether ACE-inhibitors have a specific nephroprotective effect. Since most type 2 diabetic patients do not develop diabetic nephropathy, a possible nephroprotective effect of ACE inhibitors is only relevant to the antihypertensive treatment of type 1 diabetic patients.
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PMID:[Hypertension, insulin resistance and diabetes mellitus: pathophysiological interactions and therapeutic consequences]. 198 Jul 67

The metabolic changes which accompany hyperglycemia in a person with diabetes are thought to cause renal hyperperfusion and intraglomerular hypertension, especially in the person with a predisposition to essential hypertension. Intraglomerular hypertension causing deposition of protein in the mesangium leads to glomerulosclerosis and renal failure. Screening for microalbuminuria can predict which type I diabetic patients will develop nephropathy. The decline in renal function in established diabetic nephropathy can be slowed with aggressive treatment of hypertension. The use of ACE inhibitors may also decrease intraglomerular hypertension. Whether similar treatment in the person with preclinical diabetic nephropathy would delay or prevent the onset of diabetic nephropathy is being investigated. Restricted protein intake, anti-platelet and rheolitic drugs may have a role in the treatment of established diabetic nephropathy. In end stage renal failure, renal transplantation is the treatment of choice. When transplantation cannot be performed, chronic ambulatory peritoneal dialysis is preferable to hemodialysis.
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PMID:Diabetic nephropathy: changing concepts of pathogenesis and treatment. 200 Aug 93

The effect of treatment with enalapril (10 days at 10 mg/d followed by 4 weeks at 20 mg/d) on forearm hemodynamics was assessed in eight normotensive patients and eight patients with hypertension affected by Type II diabetes as well as in eight patients with essential hypertension and normal glucose tolerance. The ACE inhibitor decreased regional vascular resistances and increased the maximum arteriolar-vasodilating capacity and venous distensibility in the three groups of patients. Thus, this study shows that ACE inhibition by enalapril improves regional hemodynamics in patients with Type II diabetes.
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PMID:The effect of ace inhibition on peripheral hemodynamics in normotensive and hypertensive patients with type II diabetes. 201 May 59


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