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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present preliminary data of a study comparing captopril, a short acting, with lisinopril, a long acting ACE-inhibitor in 8 of 12 projected patients with severe chronic heart failure (NYHA III-IV) and one additional risk factor (e.g. diabetes mellitus, renal failure). The 8 patients were treated in a cross over design for 12 weeks with either drug. While lisinopril improved NYHA-class in all patients, captopril reached this goal in only 3. Renal function was stable in all patients. Captopril influenced hormones (renin, aldosterone, norepinephrine, epinephrine) and microalbuminuria less than lisinopril. The number of adverse reactions was smaller in lisinopril treated patients. These preliminary data demonstrate at least an equal efficacy of lisinopril compared to captopril in high risk patients with severe chronic heart failure.
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PMID:[Comparison of lisinopril and captopril in treatment of severe heart failure (NYHA III-IV) in high risk patients. Preliminary results of the trial]. 185 Sep 42

If ACE-inhibitors are considered for therapy in patients with heart failure, the actual renal function has to be taken into account. In patients with reduced intravascular volume, e.g. during therapy with diuretics, the renin-angiotensin system is activated. In this situation, the renin-angiotensin-system contributes to the maintenance of arterial blood pressure and glomerular filtration rate by angiotensin II mediated vasoconstriction in vas efferens and systemic circulation. A sudden complete inhibition of the renin-angiotensin system therefore may cause a pronounced decrease in blood pressure and a reduction in glomerular filtration rate (impaired renal excretory function). In patients with heart failure concomitant chronic renal failure, the use of ACE-inhibitors is without major risk; however, the clinical efficacy may be limited. This does not apply to patients with diabetes, where the risk for impairment of renal function is increased. The potential advantage of short acting ACE-inhibitors such as captopril may clinically be relevant only in patients with very advanced severe heart failure and low arterial pressure. In any case, it is recommended to start ACE-inhibitors with a low dose and withdraw diuretics one or two days before in order to restore the intravascular volume.
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PMID:[ACE inhibition in heart failure and compromised kidney function]. 186 34

A number of studies based on animal models of both diabetes and renal insufficiency have shown that adequately reducing blood pressure attenuates the progression of glomerulosclerosis and decreases urinary protein excretion. Furthermore, compared with conventional antihypertensive therapy, angiotensin converting enzyme (ACE) inhibitors show a greater benefit in reducing these parameters. Nineteen published animal studies have investigated the effects of calcium antagonists on renal hemodynamics and glomerulosclerosis, but only three of them have evaluated the use of calcium antagonists with models of diabetes. Of six micropuncture studies based on a 1 5/6 nephrectomy model of renal insufficiency, five demonstrated reduced efferent arteriolar resistance, two showed reduced glomerular capillary pressure (PGC), and two showed significantly reduced proteinuria and glomerulosclerosis. Studies using nifedipine with both the unilaterally nephrectomized DOCA salt rat model and the 1 5/6 nephrectomy model demonstrated reduced proteinuria and glomerulosclerosis that was independent of reduced PGC. Two separate micropuncture studies of the spontaneously hypertensive rat model also found reduced efferent arteriolar resistance and PGC as well as proteinuria. Finally, studies of Dahl "salt-sensitive" rats showed an early decrease in glomerulosclerosis without a significant change in either proteinuria or glomerulosclerosis after five weeks. The results of eleven clinical studies of diabetic patients have been published; they showed divergent effects of calcium antagonists on renal function and urinary protein excretion. In the various animal models, the divergent renal hemodynamic and histologic effects reported for calcium antagonists may be largely due to the equality of blood pressure reduction, the varied baseline hemodynamic profiles, and the divergent status of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of calcium antagonists in diabetes mellitus. An overview of studies in animal models and in humans. 191 Jun 42

Treatment of hypertension in patients with NIDDM should be administered with special attention not to increase insulin resistance nor to impair insulin secretion capacity. The coexisting risk for coronary artery disease and myocardial infarction should not be increased by undesired drug effects on the plasma lipoprotein profile. Late lesions of diabetes mellitus (nephropathy, neuropathy) have also to be taken into account. Consequently angiotensin converting enzyme inhibitors, if necessary combined with calcium channel blockers, should be administered first. If blood pressure is thus not sufficiently controlled, alpha-adrenergic blockers, vasodilating agents or sympatholytics may be added. Once insulin treatment is installed, or if required for other reasons (nephropathy, congestive heart failure, cardiac arrhythmia), also diuretics and beta-adrenergic blockers are indicated in antihypertensive treatment of diabetic patients.
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PMID:[Hypertension in type II diabetes mellitus]. 195 Mar 78

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

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 Captopril Prevention Project (CAPPP) is a prospective, randomized, multi-centre intervention trial designed to investigate whether antihypertensive treatment with the angiotensin converting enzyme (ACE) inhibitor captopril may reduce cardiovascular mortality and morbidity more than a therapeutic regimen which does not include an ACE inhibitor. Secondary objectives are to compare total mortality, the development or deterioration of ischaemic heart disease, left ventricular failure, atrial fibrillation, diabetes mellitus and possible differences in renal function in the two groups. Male and female patients with essential hypertension, aged 25-66 years, will be randomly allocated to antihypertensive treatment which will comprise either the use of the ACE inhibitor captopril or will exclude all types of ACE inhibitors. Some 275 hypertension centres and health care centres in Sweden and Finland will take part in this multi-centre trial. A total of 7000 patients will be recruited and studied for an average period of 5 years, the assumption being that a 20% difference in cardiovascular mortality between the two groups can be detected with a power of 80% at the 5% significance level (two-sided test).
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PMID:The Captopril Prevention Project: a prospective intervention trial of angiotensin converting enzyme inhibition in the treatment of hypertension. The CAPPP Group. 198 Dec 18

In two cases with drug-related hyperkalemia, potassium homeostasis, causes, symptoms and therapy are discussed. Iatrogenic and therefore avoidable hyperkalemia occurs most often when potassium, ACE-inhibitors, nonsteroidal antiinflammatory drugs or potassium-sparing diuretics are administered in patients with impaired renal function or diabetes mellitus. The emergency treatment in patients with severe hyperkalemia consists of intravenous calcium injections, infusion of glucose with insulin and, more recently, salbutamol. With acidotic patients administration of sodium-bicarbonate can be tried. Ion-exchange drugs and furosemide have a more delayed effect. With oliguria and anuria hemodialysis is often necessary.
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PMID:[Hyperkalemia]. 199


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