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

Captopril is a suitable drug to treat high blood pressure in diabetic patients. This Angiotensin-Converting Enzyme Inhibitor (ACEI) is a vasodilator without tachycardia and saline retention. Furthermore, captopril is one of antihypertensive drugs with less adverse effects. It does not induce metabolic changes, improves glucose tolerance and brake the evolution of renal insufficiency. About 50-60% of patients are under control (DBP < 90 mmHg) with captopril monotherapy. In the present paper, were included 64 women and 16 men with diabetes mellitus and mild-moderate hypertension, I-II phase WHO. The average age (mean +/- S.D.) was 66.6 +/- 9.2 years. All patients were treated with 25 mg/12 h of captopril, for one month. If blood pressure was not under control, captopril treatment enhanced to 50 mg/12 h during second month. After this period of two months, patients under control were got out of this study. 37 patients (46.25%) needed a second drug. In randomized form, 20 patients associated 25 mg HCTZ one time a day (CAP + HCTZ); and 17 patients associated 20 mg/12 h of nifedipine retard (CAP + NIF). The study continued for 4 months more. Both treatments reduced blood pressure in significant form without changes statistical significant in the heart rate, weight, glycemia, cholesterol, triglycerides, c-HDL, uric acid, creatinine, Na+ and K+ blood levels. CAP + HCTZ controlled (DBP < 90 mHg) 85% and CAP + NIF 81.25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Captopril + hydrochlorothiazide versus captopril + nifedipine in the treatment of arterial hypertension in diabetes mellitus type II]. 143 67

To elucidate the important features of early renal disease in the diabetic dog, renal capillary permselectivity and fractional mesangial expansion with and without unilateral nephrectomy (NX) were examined. Pancreatectomized mongrel dogs (N = 9) received 10-20 U Regular and NPH insulin daily. Weekly blood glucose monitoring, 300 +/- 75 mg/dl (means +/- SD). Three dogs without NX had serial open needle biopsies 6-23 months post-pancreatectomy, revealing significant glomerular basement membrane widening and mesangial expansion. Without NX, inulin clearance increased from 2.55 +/- 0.89 (pre-diabetes) to 4.30 +/- 0.70 ml/min/kg body weight (N = 4, means +/- SD, p less than 0.05), whereas albuminuria, measured by radioimmunoassay, remained unchanged 2.57 +/- 1.03 (pre-diabetes) to 2.83 +/- 1.63 micrograms/min/kg body weight up to 23 months post-pancreatectomy. To determine whether altered renal capillary permselectivity occurred despite normal albuminuria, glomerular charge and size selectivity was analysed with serial fractional anionic dextran (20-44 A Stokes Einstein Radius) clearances. Furthermore, peritubular capillary permselectivity was probed with anionic and neutral 3H-dextran (26 A) using the multiple indicator dilution method. Fractional anionic dextran clearances remained unchanged up to 23 months, as did peritubular capillary permselectivity. Five diabetic dogs were compared to non-diabetic dogs with (N = 4) and without (N = 10) NX. To identify whether angiotensin II converting enzyme inhibition modified glomerular function or morphology, 3 diabetic + NX dogs received Captopril (5 mg/kg/day). At one year, diabetes + NX had an additive effect on renal hypertrophy, although fractional mesangial expansion was not enhanced by NX. Albuminuria was unaffected by NX or Captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic glomerulopathy following unilateral nephrectomy in the dog. 170 67

Normotensive patients with insulin-dependent (type I) diabetes mellitus (n = 18) were given 25 mg captopril (b.i.d.) and placebo for 3 mo in a randomized double-blind crossover study. Patients had normal renal function, and none had retinopathy. Albuminuria was less than 20 micrograms/min in 12 patients and between 20 and 200 micrograms/min in the other 6. Patients were examined at the end of the placebo and captopril phases. Captopril caused little reduction in blood pressure obtained by 24-h ambulatory monitoring (systolic 126.0 +/- 2.7 to 123.9 +/- 2.4 mmHg, P less than 0.08; diastolic 74.2 +/- 1.9 to 72.1 +/- 1.9 mmHg, P less than 0.09). Captopril lowered glomerular filtration rate from 99.5 +/- 7.7 to 71.0 +/- 5.5 ml.min-1. 1.73 m-2 (P less than 0.01), whereas renal plasma flow (443.9 +/- 15.2 ml.min-1. 1.73 m-2) remained unchanged. Filtration fraction was reduced from 22.4 +/- 1.4 to 17.4 +/- 1.4% (P less than 0.01). Urinary albumin excretion was reduced from 59.1 +/- 0.15 to 27.7 +/- 13.9 micrograms/min (P less than 0.1). Reduction was related to the extent of initial albuminuria (r = 0.997, P less than 0.001), a relationship that remained significant after logarithmic transformation (r = 0.540, P less than 0.02). Dextran clearance was used to determine glomerular capillary function. Angiotensin inhibition caused reduction in effective glomerular pore size and also reduced flow via the nondiscriminatory shunt. Angiotensin inhibition in normotensive patients with type I diabetes was well tolerated. Reduction in albuminuria is mediated by a combination of hemodynamic changes and alterations in glomerular capillary function.
Diabetes 1992 Jan
PMID:Effect of angiotensin-converting enzyme inhibition on renal function and albuminuria in normotensive type I diabetic patients. 172 41

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

Captopril (CAS 62571-86-2) may be beneficial for the treatment of diabetes because of its activating effect on peripheral glucose consumption besides its well known blood pressure degradation. The glucose oxidation has been found to be activated by captopril in thrombocytes and mononuclear leucocytes, cell types which are usually considered to be independent from insulin. Because the oxidation of pyruvate labelled in position C-1 but not of 2-14C-pyruvate and of 1-14C-acetate was enhanced, captopril most probably stimulated the pyruvate decarboxylation reaction. The metabolism of glucose labelled in positions 1 and 6 was equally activated by captopril indicating another step which may be affected by captopril.
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PMID:Influence of captopril on glucose and fatty acid oxidation in human thrombocytes and mononuclear leucocytes. 190 26

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

To assess the effects of ACE-inhibition on insulin action in Type 2 (non-insulin-dependent) diabetes mellitus associated with essential hypertension, 12 patients with Type 2 diabetes (on diet and oral hypoglycaemic agents) and arterial hypertension were examined on two occasions, in a single blind, cross-over study after two days of treatment with either captopril or a placebo. The study consisted of a euglycaemic-hyperinsulinaemic clamp (two sequential steps of insulin infusion at the rates of 0.25 mU.kg-1.min-1 and 1 mU.kg-1.min-1, 2 h each step), combined with an infusion of 3-3H-glucose to measure the rate of hepatic glucose production and that of peripheral glucose utilization. The results show that blood pressure was lower after captopril (sitting, systolic 148 +/- 5 mm Hg, diastolic 89 +/- 2 mm Hg) compared to placebo (155 +/- 6 and 94 +/- 2 mm Hg) (p less than 0.05). Captopril treatment resulted in a more suppressed hepatic glucose production (2.7 +/- 0.4 vs 4.94 +/- 0.55 mumol.kg-1.min-1), and a lower plasma non-esterified fatty acid concentration (0.143 +/- 0.05 vs 0.200 +/- 0.05 mmol/l) (captopril vs placebo, p less than 0.05) at the end of the first step of insulin infusion (estimated portal plasma insulin concentration 305 +/- 28 pmol/l); and in a greater glucose utilization (36.5 +/- 5.1 vs 28 +/- 3.6 mumol.kg-1.min-1, p less than 0.001) at the end of the second step of insulin infusion (arterial plasma insulin concentration of 604 +/- 33 pmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACE-inhibition increases hepatic and extrahepatic sensitivity to insulin in patients with type 2 (non-insulin-dependent) diabetes mellitus and arterial hypertension. 206 46

Recently the beneficial effects of captopril (angiotensin-converting-enzyme inhibitor) on diabetic nephropathy, especially proteinuria, have been reported by some investigators. The mechanism whereby proteinuria is reduced, however, have not been clarified yet. The present study was undertaken to evaluate the effects of captopril on urinary albumin excretion in relation to urinary prostaglandins (PGs) excretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Captopril (37.5 mg/day) was orally administered to 13 diabetic patients for an eight-week period. A single administration of captopril (12.5 mg) was performed in the same patients. The spot urine samples were collected in the early morning and 2 hr after the single administration of captopril. The albumin index (mg/gram-creatinine) was markedly decreased in eight patients (Group A) within four weeks, but no decrease was found in five patients (Group B). Furthermore, in Group A, by the single administration of captopril urinary excretions of 6-keto-PCF1 alpha (a stable metabolite of PGI2) and PGE2 were significantly (p less than 0.05) increased while urinary TXB2 (a stable metabolite of TXA2) excretion did not change significantly. The urinary 6-keto-PGF1 alpha/TXB2 ratio, which is significantly (p less than 0.05) low in diabetic patients was significantly (p less than 0.01) increased up to the normal value in Group A. In Group B, however, there were no significant changes in urinary PGs excretion. These results suggest that captopril enhances the production of intrarenal vasodilatory PGs such as PGI2 and PGE2, which may be deeply involved in the reduction of intraglomerular capillary pressure and urinary protein excretion in diabetic patients.
Diabetes Res 1990 Mar
PMID:Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy. 209 82

Diabetes-associated hypertension is accompanied by high levels of body sodium and cardiovascular hyper-reactivity to noradrenaline. Captopril, a promising drug for the treatment of hypertension in diabetics, may influence sodium metabolism and adrenergic pathways. This possibility was investigated in 11 patients with non-azotaemic diabetes mellitus and hypertension, studied after a 3-week placebo phase and after an 8-week phase of captopril treatment (50-100 mg/day). Blood pressure, exchangeable body sodium, blood volume, plasma renin activity, angiotensin II (Ang II), aldosterone, catecholamine levels and the pressor reactivity to infused Ang II or noradrenaline were measured. Compared with placebo, captopril caused a significant decrease in arterial pressure and stimulation of plasma renin activity. Exchangeable sodium, blood volume, plasma Ang II, aldosterone, noradrenaline and adrenaline levels, the pressor and aldosterone responsiveness to infused Ang II and the pressor response to infused noradrenaline (alone or combined with atropine) were not modified. These findings suggest that in hypertensive diabetics angiotensin converting enzyme inhibition causes a marked decrease in blood pressure. The mechanism of action is unrelated to changes in body sodium or noradrenergic-dependent pressor reactivity. In the stable phase of therapy, Ang II-dependent pathways are left unaltered when captopril is administered twice a day.
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PMID:Cardiovascular regulation during angiotensin converting enzyme inhibition with captopril in diabetes-associated hypertension. 216 58

Captopril decreases protein excretion in patients with nephrosis. To evaluate whether captopril has an acute antiproteinuric effect and to evaluate the role of changes in renal hemodynamics or glomerular permselectivity on this effect, renal clearance studies were performed in patients without diabetes but with nephrosis. Protein excretion and renal hemodynamics were measured at baseline and after the administration of captopril. To measure the contribution of renal prostaglandins, patients were restudied on a separate day, after the combined administration of captopril and the prostaglandin synthetase inhibitor ibuprofen. Both treatments significantly reduced mean protein excretion, but the change was greater with combined therapy than with captopril alone (40.6% vs 20.0%). Mean glomerular filtration rate (GFR) decreased by 4.8% (not significant) and 16.5% (p less than 0.001), and filtration fraction (FF) decreased by 13.6% (p less than 0.001) and 14.9% (p less than 0.001) after captopril alone and combined therapy, respectively. No significant correlation was found between changes in proteinuria and changes in GFR or FF after treatment with captopril alone. In contrast, the decrease in proteinuria correlated with the change in GFR after combined drug administration (r = 0.68, p = 0.06). The ratio of immunoglobulin G to albumin clearance, an index of glomerular permselectivity, was unaffected by captopril but decreased significantly (by 43%) after combined drug administration. The results suggest that the acute antiproteinuric effect of captopril is not due to changes in FF, GFR, or glomerular perselectivity. The addition of ibuprofen enhances the antiproteinuric effect of captopril by decreasing the GFR as well as by enhancing the permselectivity of the glomerular capillary membrane.
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PMID:Acute effects of captopril and ibuprofen on proteinuria in patients with nephrosis. 221 55


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