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

We conducted a prospective evaluation of the effects of chronic captopril therapy on glucose tolerance in 8 nondiabetic, hypertensive patients and 6 hypertensive patients with impaired glucose tolerance, including 3 diabetic patients. Captopril was well tolerated by all patients, and no untoward effects were observed. Chronic captopril therapy produced a significant decrease in blood pressure in all patients. No patients with normal glucose tolerance developed diabetes mellitus. Neither fasting nor post-glucose-load venous plasma glucose deteriorated in any patients during chronic captopril therapy. There were no significant changes in the insulinogenic index (delta IRI/delta BS at 30 min post-glucose load) in patients with either normal or impaired glucose tolerance. These results suggest that, in addition to its antihypertensive effect, chronic captopril therapy does not compromise glucose metabolism in hypertensive patients. Thus, captopril may have a clinical advantage in that it apparently can be given safely to hypertensive patients with either normal or impaired glucose metabolism.
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PMID:Glucose tolerance during chronic captopril therapy in patients with essential hypertension. 243 93

It has been suggested that the metabolic side effects of antihypertensive drugs are responsible for their failure to reduce cardiovascular morbidity in patients with hypertension. Therefore, in 50 patients with essential hypertension, we performed a randomized, double-blind, crossover study comparing the effects of carbohydrate and lipid metabolism of captopril (mean [+/- SD] dose, 81 +/- 24 mg per day) and hydrochlorothiazide (40 +/- 12 mg per day) over two four-month treatment periods. Captopril increased the insulin-mediated disposal of glucose, as compared with placebo, from 5.7 +/- 2.4 to 6.3 +/- 2.5 mg per kilogram of body weight per minute (P less than 0.05), whereas hydrochlorothiazide caused a decrease from 6.4 +/- 2.0 to 5.7 +/- 1.9 (P less than 0.01). Captopril had no effect on the basal insulin concentration, but it decreased the late (30- to 90-minute) insulin response to glucose and increased the early (2- to 6-minute) insulin peak. Hydrochlorothiazide increased the basal insulin concentration and the late insulin response to glucose. These findings may be explained by an increase in insulin sensitivity with captopril and a decrease with hydrochlorothiazide. Little or no change was seen in serum lipid or lipoprotein levels during treatment with captopril, whereas hydrochlorothiazide caused significant increases in serum total (5 percent) and low-density lipoprotein (6 percent) cholesterol levels and total (15 percent) and very-low-density lipoprotein (25 percent) triglyceride levels, as compared with placebo (P less than 0.01 for all comparisons). We conclude that hydrochlorothiazide for the treatment of essential hypertension has adverse effects on glucose and lipid metabolism. It is possible, but not proved in this study, that these changes may contribute to the risk for diabetes mellitus and coronary heart disease. In contrast, captopril appears to have beneficial or no effects on glucose and lipid metabolism.
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PMID:A comparison of the effects of hydrochlorothiazide and captopril on glucose and lipid metabolism in patients with hypertension. 240 56

Effective renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed in early insulin dependent diabetics (duration of diabetes less than 10 yr) during short term administration of angiotensin converting enzyme inhibitor. In a double blind randomized study, RPF and GFR were measured in normotensive normoalbuminuric (albumin excretion rate less than 20 micrograms/min) male IDDs before and after two weeks of Captopril 25 mg bd (n = 6) or placebo (n = 6). RPF and GFR were measured by means of a primed constant infusion of 125I iodohippurate and 51CR EDTA, respectively and corrected for 1.73m2 surface area. Supine blood pressure was measured throughout the study period. Mean (+/- SE) systolic and diastolic blood pressures were unchanged in both groups of subjects, being 124 +/- 5 mmHg and 78 +/- 4 mmHg before and 126 +/- 5 mm and 81 +/- 4 mm during Captopril and 121 +/- 6 mm and 79 +/- 4 mm before and 120 +/- 5 mm and 80 +/- 3 mm during placebo administration. RPF and GFR remained unchanged during Captopril administration, from 719 +/- 28 ml/min and 148 +/- 6 ml/min prior to and 721 +/- 26 ml/min and 149 +/- 6 ml/min during therapy. Similarly RPF and GFR were unchanged in the placebo treated group at 634 +/- 24 ml/min and 143 +/- 5 ml/min before end 630 +/- 28 ml/min and 140 +/- 7 ml/min after two weeks. Glycaemic control was unchanged in either group during the study period.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1989 May
PMID:Renal haemodynamics during short-term angiotensin converting enzyme inhibition in normotensive normoalbuminuric insulin dependent diabetics. 269 80

The effect of captopril monotherapy on blood pressure and metabolism was investigated in a placebo-controlled study in 30 non-insulin dependent (Type II) diabetic subjects during a 3-week observation period (run-in/drug; placebo/wash-out) on a metabolic ward. Captopril significantly reduced both systolic and diastolic blood pressure (154/90 +/- 5/2 vs. 144/86 +/- 4/3 mmHg) without major side effects. Mean run-in postprandial blood glucose concentrations were also reduced upon ACE-inhibition (9 a.m.: 12.7 +/- 0.4 vs. 11.1 +/- 0.4 mmol/l; 1 p.m.: 11.0 +/- 0.3 vs. 8.9 +/- 0.3 mmol/l; P less than 0.05), while blood kinin concentrations (40.0 +/- 2.5 pmol/l) were approximately doubled (108.8 +/- 23.5 pmol/l; P less than 0.05). Body mass index, fasting plasma insulin, serum electrolyte pattern, uric acid, white blood count, lipid profile as well as hepatic and renal function parameters remained unaltered throughout the observation period. The data are in line with recent experimental studies showing a beneficial metabolic effect of captopril in Type II diabetes. ACE inhibitors might therefore become first-line drugs in early antihypertensive intervention in Type II diabetic patients.
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PMID:Role of angiotensin-converting enzyme inhibitors in early antihypertensive treatment in non-insulin dependent diabetes mellitus. 307

The aim of this study was to evaluate the effect of captopril on carbohydrate metabolism in diabetic patients with essential arterial hypertension. Sixteen patients with non-insulin-dependent diabetes mellitus and hypertension were studied. Captopril was employed in different doses, and where patients receiving 100 mg/day remained hypertensive, hydrochlorothiazide 50 mg/day was added. Treatment was maintained for 90 days in 14 patients, 2 being excluded because of side effects. Basal blood pressure was normalized in 8 patients (57%) with captopril alone, and in 6 patients (43%) following the addition of hydrochlorothiazide. Basal glucose levels were not altered. Oral glucose tolerance tests performed during captopril treatment showed a lower glucose response, without changes in the insulin response. There was significant weight loss during the study. We conclude that captopril appears to be a safe treatment in essential hypertension associated with non-insulin-dependent diabetes mellitus, producing no deleterious effects on metabolic control.
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PMID:Effect of converting enzyme inhibitors in hypertensive patients with non-insulin-dependent diabetes mellitus. 353 65

This investigation was performed in two groups of adult patients, 10 with type I and 10 with type II diabetes mellitus, all with arterial hypertension (160 to 200 mm Hg systolic and 95 to 120 mm Hg diastolic). Captopril, 50 mg twice a day, was administered for 12 weeks and was effective as monotherapy in 16 patients. Mean arterial pressure (+/- s.d.) in type I patients changed from 121.4 +/- 9.6 to 100.2 +/- 10.1 after 4 weeks and to 102.0 +/- 3.8 mm Hg after 12 weeks; in type II patients it changed from 132.8 +/- 5.7 to 123.9 +/- 13.5 after 4 weeks and to 109.1 +/- 11.1 mm Hg after 12 weeks. The differences were statistically significant. In only 4 patients was it necessary to add a thiazide after the first month of therapy. No significant change was induced by captopril in urine output, osmolar clearance, free water clearance inulin, and PAH clearances. No significant change was observed in serum and urine Na+, Cl-, Ca++ and Mg++, whereas a statistically significant reduction was found in the renal clearances of K+ and PO4-. No important change in serum aldosterone was found, while plasma renin activity was increased, as expected. No alterations in urine protein, glucosaminoglycans, gamma GT, and N-acetyl-beta-glucosaminidase were observed during follow-up. All patients maintained good metabolic control of their disease. No neutropenia and orthostatic hypotension were seen. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients, without affecting renal function, electrolyte balance and the metabolic control of diabetes.
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PMID:Captopril in the treatment of hypertension in type I and type II diabetic patients. 353 66

The apparently excellent pharmacological properties of Captopril as treatment for insulin-dependent and other hypertensive diabetics of all ages were investigated at a Diabetes Centre. Fifteen out-patients receiving oral hypoglycaemic drugs or insulin and suffering from slight or moderate hypertension (diastolic AP: 95-115 mmHg) were selected for treatment. The Captopril was administered in daily doses of 50 or 100 mg for 60 days. Tests on the 30th and 60th days revealed a statistically significant reduction in max/min OAP values, but no statistically significant variations in either cardiac frequency or glycaemia before and after meals. Nor did the main haematochemical parameters show any significant alteration.
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PMID:[Treatment of hypertension in the diabetic with captopril]. 388 42

Depressed baroreflex sensitivity (BRS) after acute myocardial infarction (AMI) is considered an indication of decreased vagal and/or increased sympathetic tone. To determine the effect of angiotensin converting enzyme inhibitors (ACEI) on BRS after AMI we studied 27 patients with a first Q wave AMI, no signs of heart failure and no history of arterial hypertension or diabetes mellitus. An additional group of 10 patients with the same clinical characteristics served as controls. On the 5th day after the onset of AMI, three consecutive boluses of phenylephrine were given intravenously and baseline BRS was taken as the mean slope of the linear regression lines of RR intervals over systolic blood pressure. QT interval was also measured and corrected according to Bazett's formula (QTc). Consequently, a single oral dose of captopril 50 mg or placebo was given to treatment or control group patients, respectively; BRS and QTc were reassessed 1 h later. One hour after captopril administration BRS increased from 5.95 +/- 2.80 to 9.14 +/- 3.46 ms.mmHg-1 (P < 0.0001); QTc increased from 414 +/- 46 to 425 +/- 46 ms (P < 0.0001), systolic blood pressure decreased from 125 +/- 19 to 115 +/- 15 mmHg (P = 0.0002), while heart rate did not change significantly. Baseline BRS was correlated only with age (r = -0.74, P < 0.0001). In the control group, 1 h after placebo, no difference was observed in any variable compared to baseline. Captopril appears to improve BRS immediately in the early phase of AMI.
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PMID:Acute effect of captopril administration on baroreflex sensitivity in patients with acute myocardial infarction. 749 6

The present study assessed the extent to which remission of nephrotic-range proteinuria occurred in patients with Type I diabetes enrolled in the Captopril Study, a placebo controlled multicenter clinical trial of captopril therapy in diabetic nephropathy. Of the 409 patients recruited into the Captopril Study, 108 had nephrotic-range proteinuria (> 3.5 g/24 hr) at entry in the Study (baseline). This group was the subject of the present study. Remission of nephrotic-range proteinuria was defined as follows: (1) Onset of the remission was taken as the date when proteinuria was first noted to be < or = 1.0 g/24 hr. (2) The reduction in proteinuria had to be sustained for a minimum of six months and until the end of the Captopril Study. (3) During the remission, the average of all 24 hour proteinuria measurements could not exceed 1.5 g. (4) Decline in renal function could not explain the reduced proteinuria. That is, the patient's serum creatinine during the entire period of observation in the Captopril Study had to remain at less than a doubling of the baseline serum creatinine. Remission of nephrotic-range proteinuria occurred in 7 of 42 patients assigned to captopril (16.7%, mean follow-up 3.4 +/- 0.8 years) and in 1 of 66 patients assigned to placebo (1.5%, mean follow-up 2.3 +/- 1.1 years; P = 0.005, comparing remission rate in captopril vs. placebo-treated patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Remission of nephrotic range proteinuria in type I diabetes. Collaborative Study Group. 770 28

Captopril given in dosages of 25 mg reduced the doubling of serum creatinine levels by 48% in patients with insulin-dependent diabetes mellitus. Intensive insulin therapy in patients with IDDM delays the onset and slows the progression of diabetic nephropathy, retinopathy, and neuropathy.
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PMID:Nephrology. 775 21


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