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

Renal functional reserve capacity was evaluated in 19 normotensive type I diabetics without microalbuminuria. All patients had normal basal renal function as assessed by 24-hour creatinine clearances higher than 120 ml/min. PAH, inulin, and creatinine clearances were carried out every hour before, during, and after infusion of an amino acid (AA) solution. The same experiment was repeated after ACE inhibition with captopril (25 mg). Two groups of patients were found: Group A (responders) showed a significant rise in GFR after AA infusion (inulin clearances from 117 +/- 8 to 138 +/- 10 ml/min) (p less than 0.05), whereas in Group B (non-responders) no significant change in GFR was observed. Groups were comparable in age, duration of diabetes, metabolic control, and mean arterial blood pressure. Group B, however, had a significantly higher basal inulin clearance (167 +/- 17 ml/min) than Group A (117 +/- 8 ml/min). In Group A ACE inhibition completely blocked the AA-induced rise in GFR, while basal GFR in Group B was significantly reduced (167 +/- 17 to 148 +/- 8 ml/min) after captopril administration. In both groups renal plasma flow was enhanced by ACE inhibition. A rise in glucagon was observed in all patients during AA infusion. It is concluded that type I diabetics with normal basal renal function already have reduced (Group A) renal functional reserve capacity, which is completely abolished (Group B) when concomitant hyperfiltration occurs. ACE inhibition reduces hyperfiltration and is capable of blocking the AA-induced rise in GFR in these patients.
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PMID:[Behavior of the renal functional reserve in type I diabetic patients: effect of ACE-inhibition]. 221

It is known that mild hypertension is a common disorder and there is increasing evidence that it is possible to decrease the incidence of cardiovascular damage by antihypertensive treatment. Stimulated by the controversy on the identification and treatment of patients with mild hypertension, a Dutch hypertension consensus meeting was held on March 16th 1990. Consensus was reached that the decision to treat should be taken on the basis of both the blood pressure level and the individual risk profile, including hypercholesterolaemia, history of smoking, diabetes, or a family history of cardiovascular disease. Subjects at risk should be identified by selective case finding (persons with known additional risk factors) and screening restricted to men aged 55 to 65 years. All patients should be started on non-pharmacological treatment by decreasing sodium intake, and where necessary reducing body weight and alcohol consumption, and stopping smoking. If antihypertensive drugs are to be given, diuretics, beta-blockers, ACE-inhibitors, and (or) calcium antagonists are the drugs of choice.
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PMID:[Hypertension consensus in The Netherlands]. 223 88

Renal dysfunction and hypertension are closely associated. Hypertension causes approximately 25% of end-stage renal disease (ESRD) and develops in virtually every patient with advanced renal insufficiency from any cause. Although normalization of blood pressure can reduce mortality from uremia and ameliorate the progression of renal impairment in patients with established renal insufficiency from hypertension and diabetes, antihypertensive therapy alone is not totally effective in preventing progressive compromise of renal function--especially in blacks and diabetics, who are at high risk for developing ESRD. Of particular promise is the rapidly increasing understanding of the intrarenal autocrine and paracrine functions of angiotensin II produced locally by a tissue renin-angiotensin system. Consistent and convincing experimental data have demonstrated that angiotensin II plays many roles in the control of renal function and the kidney's response to injury. The intrarenal effects of angiotensin II include: 1) increase in the efferent arteriolar tone, resulting in increased glomerular capillary pressure, 2) promotion of mesangial cell contraction, 3) stimulation of proximal tubular Na+ reabsorption, and 4) possible growth hormone effects leading to hypertrophy or hyperplasia of vascular smooth muscle. Because of their favorable intrarenal hemodynamic effects (particularly reduction of glomerular capillary pressure), ACE inhibitors may provide a renal protective effect in addition to their systemic antihypertensive effects. Clinical trials evaluating the effect of ACE inhibition on the progression of renal insufficiency in hypertensives and diabetics are currently under way. Favorable results could lead to a significant decrease in the morbidity and mortality associated with hypertension.
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PMID:Renal protective effects of angiotensin converting enzyme inhibitors. 226 Nov 45

Joint studies of the ALIMDA and Society of Actuaries, notably those of 1935, 1959 and 1979, established that there is a progressive rise in cardiovascular mortality with successive increments in blood pressure. This has provided the basis of underwriting. The converse is not true, or at least has not been true until very recently. Drugs that effectively reduce blood pressure have been available for several decades, but reduction and maintenance of blood pressure is still accomplished in only a minority of hypertensives. Long-term trials employing a combination of drugs, i.e., diuretics, vasodilators and reserpine and subsequently beta-blockers, almost without fail have not shown that treatment with these agents significantly reduces heart disease mortality and sudden death. This has been attributed, perhaps without basis, to an unfavorable countering effect of increased lipid levels, aggravating this risk factor, and other undesirable metabolic effect of diuretics, such as hypokalemia and depletion of body magnesium, increasing the propensity to ventricular arrhythmias, hyperglycemia, worsening diabetes, and hyperuricemia. A survey of 674 persons with hypertension seen personally during the period 1985-89, who were under the care of approximately that many physicians, reveals striking changes in drug prescription and use during this brief period that portend a major change in the outlook of hypertension. Two classes of drugs have increased rapidly in popularity: these are the angiotensin-converting enzyme inhibitors (ACE inhibitors) and the calcium blockers. Both classes of drugs effectively lower blood pressure and have minimal side effects with good compliance. They act not only to reduce peripheral vascular resistance, but also locally in the heart muscle to directly cause left ventricular hypertrophy to regress, an effect of great consequence. The drugs used in former trials such as the vasodilators and diuretics have no effect on left ventricular hypertrophy, unlike the ACE inhibitors and calcium antagonists. Left ventricular hypertrophy is the key lesion in hypertension and is only in part due to increased work load imposed by elevated pressure. It is associated with elevated blood pressure, but not closely and occurs independently; ventricular myocytes as well as myocytes of the vasculature being stimulated to growth by angiotensin and calcium, potentiating the effect of norepinephrine. Left ventricular hypertrophy greatly increases the propensity to ventricular arrhythmias and sudden death, and is a prime cause of cardiac mortality and sudden death not only in hypertension, but also in obesity, aging and diabetes, in which conditions left ventricular hypertrophy also is very common.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Major new developments affecting treatment and prognosis in hypertension. 235 5

A relative systemic hyperinsulinism, sodium retention as well as an increased cardiovascular reactivity to norepinephrine and angiotensin II in diabetics may explain the prognostically unfavorable frequent association of diabetes with high blood pressure. The first therapeutic approach against hypertension is omission of smoking and exaggerated alcohol consumption as well as of drugs which elevate blood pressure. An attempt to reach a normal body weight by means of a sodium restricted diabetes-diet is next. If blood pressures remain elevated an antihypertensive drug is prescribed in monotherapy, nowadays preferably a calcium antagonist or an ACE-inhibitor, because both of them cause few side effects, do not impair glucose and lipid homeostases and are easy to handle with a once-a-day regimen. A therapeutic algorithm is presented and consideration of the total risks of morbidity and mortality in these patients stressed.
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PMID:[Antihypertensive therapy in patients with diabetes mellitus]. 240 85

ACE-inhibitors exhibit their blood pressure-lowering activity not only via a reduction of angiotensin II but also via on increase of kinin levels. The latter are known to improve insulin action and hence carbohydrate metabolism in normal volunteers and diabetics. Accordingly, ACE-inhibitors display the same effects. As clinical trials show they are especially useful for the treatment of hypertension in diabetes mellitus.
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PMID:[ACE-inhibitors and glucose metabolism]. 240 49

1. Streptozotocin diabetes was induced in Wistar-Kyoto rats fed a 50% protein diet. Animals were randomized to receive either the ACE inhibitor ramipril, 1 mg/L in drinking water (n = 7), or no treatment (n = 7) and were studied for 6 months. Blood glucose, body weight and glomerular filtration rate (GFR) were measured at 0, 1, 4, 8 and 16 weeks of diabetes and urinary albumin excretion was measured every 8 weeks. 2. In both groups, GFR increased significantly within 1 week of induction of diabetes (P less than 0.001) and thereafter remained stable. There was no difference in GFR between the treated and untreated groups. 3. Urinary albumin excretion increased progressively in both groups throughout the study. Ramipril treatment reduced albuminuria by approximately 50% at weeks 16 and 24 (P less than 0.01). 4. The amelioration of diabetic albuminuria by ACE inhibition, in the setting of high dietary protein intake, may have important implications for the treatment of human diabetic nephropathy.
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PMID:Ramipril reduces albuminuria in diabetic rats fed a high protein diet. 252 67

This report describes the case of a 70-year-old female suffering from diabetes mellitus and dilatative cardiomyopathy with congestive heart failure. It is likely that alveolar-capillary membrane damage occurred apart from cardiac involvement. Diffuse interstitial pulmonary fibrosis subsequently occurred with consequent acute progressive respiratory failure and death. The cause of the damage to the alveolar-capillary membranes is still unknown and we thought that long-term administration of captopril might have contributed to the damage itself, since like all ACE-inhibitors, captopril is able to bring about tissular storage of both bradykinin and prostaglandins and therefore alter the pulmonary reactivity to phlogistic stimuli.
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PMID:[Acute progressive respiratory insufficiency caused by diffuse interstitial pulmonary disease in a diabetic patient with dilated myocardiopathy]. 270 34

In view of the pharmacological and chemical reasons for using ACE-inhibitors to treat diabetic hypertension, a group of 40 outpatients were treated with Enalapril. The sample consisted of 20 outpatients, 6 males, 14 females aged 48-76 (mean age 63.75), 18 of whom had type II and 2 type I diabetes and 11 under treatment by diet and hypoglycaemic drugs or insulin. All these patients presented slight or moderate essential arterial hypertension (diastolic pressure less than 115 mmHg). For about one year 17 of the patients were given 20 mg/die Enalapril and the remaining three 10 mg/die in a single morning dose. In 16 cases no other treatment was given. In 4 a non-potassium conserving diuretic was also given. Check-ups before six months into and at the end of treatment showed: a statistically significant reduction in systolic (p less than 0.05) and diastolic (p less than 0.01) pressure. In contrast no significant change was noted in heart beat, glycaemia before or after meals, body weight, glycosylated haemoglobin or any other blood chemical parameter considered. In one case only there was a slight increase in proteinuria that was however present at the start of treatment. As far as side effects are concerned there was one case of cardiac palmus during treatment and one case of coughing that regressed totally when treatment was suspended but nothing else of significance. It should be noted that the antidiabetic treatment remained unchanged throughout the period considered in most cases and at most was subjected to minimal qualitative and quantitative adjustments.
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PMID:[Prolonged treatment of hypertension in diabetic patients with enalapril. 1-year follow-up]. 282 79

The purpose of this study was to evaluate the effects of the ACE inhibitor enalapril (E) on blood pressure and metabolic control in 15 hypertensive patients with non-insulin-dependent diabetes mellitus. When the treatment goal was not reached with enalapril alone, hydrochlorothiazide (HCTZ) was added. A diastolic blood pressure (DBP) below 90 mmHg was achieved in seven patients with enalapril alone (47%), and in an additional four (27%) with concomitant hydrochlorothiazide. No significant adverse effects of enalapril occurred and all patients completed the study. Monotherapy with enalapril did not affect metabolic control or renal function. Addition of HCTZ to E did not consistently result in further lowering of blood pressure and caused deterioration of both the degree of metabolic control and renal function. We, therefore, conclude that monotherapy with enalapril can be a safe and satisfactory treatment for hypertensive patients with NIDDM. Caution is needed, however, when HCTZ is added, since this may adversely affect metabolic control and renal function whereas the effect on blood pressure may be variable.
Diabetes Res 1988 Sep
PMID:Effects of enalapril with and without hydrochlorothiazide in hypertensive patients with non-insulin-dependent diabetes mellitus. 285 59


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