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

20 patients with essential hypertension and diabetes mellitus (DM) type II were given Capoten (100-125 mg/day for 6 weeks) followed in a 2-week interval after its course termination by ramipril (10.0-12.5 mg/day). 50% of patients were sensitive to Capoten, 50% were resistance: 35 and 40% to ramipril, respectively. Ramipril was discontinued because of toxicity in 25% of patients. Hypotensive effects of ramipril were weaker than Capoten, though the former drug appeared more potent in lowering of peripheral vascular resistance at rest and at reactive hyperemia. Vasodilatation did not differ much.
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PMID:[A comparison of the effect of Capoten (captopril) and ramipril on the circadian profile of the arterial pressure and peripheral hemodynamics in patients with hypertension combined with diabetes mellitus]. 908 6

In several studies organ protective effects of ACE inhibitors independent from their antihypertensive action have been demonstrated. The mechanisms of the protective effects of angiotensin converting enzyme (ACE) inhibitors on vasculature and kidney are largely unknown. In the present study the modulatory action of captopril on the angiotensin II (AngII), arginine vasopressin (AVP), and platelet derived growth factor (PDGF)-induced increase of cytosolic free calcium concentration ([Ca2+]i) was investigated in cultured vascular smooth muscle cells (VSMC) and cultured glomerular mesangial cells (MC) from rats using the fluorescent dye technique. Resting [Ca2+]i in VSMC or MC was not significantly affected by captopril. The preincubation of VSMC with 1 mumol/l captopril significantly reduced the AngII-induced [Ca2+]i increase in VSMC from 90 +/- 10 nmol/l (n = 78; mean +/- SEM) to 51 +/- 16 nmol/l (n = 53; p < 0.05) and in MC from 102 +/- 42 nmol/l (n = 14) to 43 +/- 12 nmol/l (n = 7; p < 0.05). In the absence of extracellular calcium captopril produced no effect on AngII induced changes of [Ca2+]i. Captopril significantly attenuated the AVP-induced [Ca2+]i increase in VSMC and MC. The preincubation of MC with 1 mumol/l captopril for 40 min significantly reduced the PDGF-induced [Ca2+]i increase in MC from 127 +/- 31 nmol/l (n = 11) to 61 +/- 32 nmol/l (n = 5, p < 0.05). The present results may indicate that part of the protective effects of ACE inhibitors on vasculature and kidney may be promoted by inhibition of growth-factor induced changes of calcium homeostasis.
Exp Clin Endocrinol Diabetes 1997
PMID:Cellular protective action of angiotensin converting enzyme inhibitors. 928 48

In three prospective cohort studies, treatment with beta-blockers and diuretics has been associated with an increased risk of diabetes developing. Prospective, randomized studies with antihypertensive drugs have demonstrated differences between different classes of drugs regarding effects on insulin sensitivity. Thus, treatment with beta-blockers or diuretics is associated with impairment in insulin sensitivity, whereas most modern calcium-channel blockers and angiotensin-converting enzyme (ACE) inhibitors are neutral. However, there are exceptions within the different classes. Captopril seems to differ from the other ACE inhibitors in that the result is an improvement of insulin sensitivity. In the Captopril Primary Preventive Project the effects on cardiovascular disease and diabetes of captopril-based and conventional treatment are compared. This study will hopefully give the answer to the question whether insulin resistance is a valid intermediary endpoint.
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PMID:Insulin resistance as an intermediary endpoint. 949 38

Nine months after cadaveric renal transplantation the nephrotic syndrome developed in a patient with insulin-dependent diabetes. Renal biopsy ruled out tissue lesions induced by cyclosporine, chronic rejection, recurrence of diabetic kidney disease and de novo glomerulopathies. Captopril-enhanced nephrography and a high plasma renin response suggested renal artery disease. Angiography revealed five intrarenal arterial stenoses. Four were successfully dilated with a prompt diuretic response and diminished proteinuria. Late angiography showed a moderate restenosis in two of the dilated arteries. Due to persistent proteinuria, elevated blood pressure and higher serum creatinine levels than at nadir after transplantation low-dose ACE inhibitor therapy was started. This normalized proteinuria, blood pressure and serum creatinine levels. This beneficial response to combined renal artery balloon angioplasty and medical treatment has been sustained for 2.5 years.
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PMID:Nephrotic syndrome, hyperreninemia and multiple transplant renal arterial stenoses in a patient with diabetes. 957 75

The metabolic affects of anapriline, captopril, and clophelin were studied in the blood and liver homogenates ex vivo and in vitro in experiments on intact rats and rats with alloxan diabetes. Anapriline lowered the blood lactate content in rats with diabetes and intact rats, reduced the level of glycemia in animals with marked hyperglycemia. Captopril increased the blood insulin and lactate content in rats with diabetes and the content of pyruvate in vivo. The results of the study show that the use of clophelin and anaprilin in the treatment of patients with diabetes mellitus is most rational.
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PMID:[The effect of antihypertensive preparations on carbohydrate metabolism in intact rats and in alloxan diabetes]. 969 78

Thirty-four patients (65.3+/-3.3 years of age, mean+/-SEM) with hyperkalemia (serum potassium >5.0 mEq/L) had measurement of their renin-aldosterone system. Nineteen patients (56%) had plasma renin activity (PRA) >1.5 ng/mL/h, which was not low, while 15 (44%) had PRA <1.5. Twelve of the 15 hyporeninemic hyperkalemic patients were studied to determine whether their renin-aldosterone system responded to 2 weeks of furosemide, 20 mg daily. Four were nonresponders: PRA averaged 0.3+/-0.1 ng/mL/h, and it did not increase with furosemide or respond to captopril before or after furosemide. Eight patients were responders: PRA averaged 0.6+/-0.2 ng/mL/h and increased with furosemide to 5.5+/-3.4 ng/mL/h. Captopril failed to increase PRA before furosemide, but PRA increased to 15.3+/-8.4 ng/mL/h after furosemide. Plasma aldosterone was low in both nonresponders and responders (3.5+/-1.2 ng/dL vs 5.8+/-2.5 ng/dL) and did not increase significantly with furosemide (4.3+/-1.7 ng/dL vs 8.7+/-2.5 ng/dL). Serum potassium did not fall and therefore did not limit the rise in aldosterone. Renin responders had greater body weight, were predominantly female (6/8 vs 2/4) and were more likely to have diabetes mellitus (7/8 vs 0/4). Plasma atrial natriuretic peptide (ANP) fell with furosemide in 8 of 8 responders and in 1 of the 2 nonresponders in whom it was measured. Neither group had suppressed plasma prorenin levels, indicating no suppression of renin gene expression. These results indicate that many hyperkalemic patients do not have suppressed PRA. Further, a majority of patients with suppressed PRA have high levels of ANP and can respond to diuretic therapy with a rise in PRA and a fall in ANP, suggesting physiologic suppression of the renin system by volume expansion. A minority of hyperkalemic patients with suppressed PRA had PRA that did not increase under these study conditions.
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PMID:Renin-aldosterone system can respond to furosemide in patients with hyperkalemic hyporeninism. 973 29

Effect of two angiotensin convertase inhibitors, enalapril and captopril, on blood plasma and erythrocyte lipid peroxidation and plasma peroxyl radical-trapping capacity was studied in rats with streptozotocin-induced diabetes. A progressive increase in blood erythrocyte malondialdehyde (MDA) level was observed in diabetic rats after 6 and 12 weeks. Blood plasma MDA level increased while plasma peroxyl radical-trapping capacity was decreased after 12 weeks. Captopril (2 mg/kg body weight) augmented the diabetes-induced changes in MDA content after 6 weeks and prevented them after 12 weeks increasing also the peroxyl radical-trapping capacity. Enalapril (1 mg/kg body weight) counteracted the diabetes-induced changes in MDA content after both 6 and 12 weeks but did not affect the plasma peroxyl radical-trapping capacity. These results suggest a possibility of a therapeutic use of angiotensin convertase inhibitors to attenuate the effects of oxidative stress in diabetes.
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PMID:Effect of angiotensin convertase inhibitors on lipid peroxidation and peroxyl radical-trapping capacity in rats with experimental diabetes. 973 55

POSSIBLE INTERACTIONS: Converting enzyme inhibitors (CEI) can intensify the glucose lowering effect of insulin or sulfonureas. This interaction has been observed in a few clinical cases and studied systematically in regional pharmacovigilance centers. LOW RISK RATE: This interaction occurs in certain patients with well-controlled diabetes who are given a CEI or when CEI dosage is increased. The risk of hypoglycemia in diabetics treated with CEI is very low and can be considered as negligible compared with the benefit of this class of well-tolerated renal-protective antihypertension agents. DRUG DEPENDENT: A larger number of cases of hypoglycemia have been reported with captopril and enalapril, probably because these two CEI have been marketed for a longer period. Captopril may have a stronger hypoglycemia effect than enalapril. It has been demonstrated with hyperinsulin euglycemic clamp that captopril improves sensitivity to insulin in healthy volunteers with normal blood pressure; with enalapril however, the increase in insulin sensitivity is less pronounced and non-significant. AN INDIRECT MECHANISM: Captopril, and to a lesser extent enalapril, indirectly increases insulin sensitivity by increasing circulating kinine which leads to vasodilatation in the muscles and increased glucose uptake in muscle tissue.
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PMID:[Interaction between converting enzyme inhibitors and hypoglycemic sulfonamides or insulin]. 985 70

The effects of two weeks of oral administration of the angiotensin-converting enzyme inhibitors captopril (a sulphydryl-containing drug) and enalapril (which lacks the sulphydryl group) on skeletal muscle glucose uptake, arterial blood pressure, cardiac hypertrophy, proteinuria and aortic vascular reactivity in obese Zucker rats were evaluated. Captopril (50 mg kg(-1) once daily) and enalapril (10 mg kg(-1) did not modify body weight gain or food or water intake. Both drugs decreased systolic blood pressure (157+/-6, 133+/-4 and 136+/-3 mm Hg, in vehicle-, captopril- and enalapril-treated rats, respectively), blood glucose (172+/-8 vs. 151+/-7 and 158+/-5 mg dl(-1), respectively), proteinuria (46+/-10 vs. 17+/-2 and 18+/-2.5 mg dl(-1), respectively) and heart weight (2.17+/-0.03, 1.98+/-0.02 and 1.99+/-0.04 mg g(-1)of body weight, respectively). Plasma insulin concentration was significantly increased by enalapril (17+/-2 ng ml(-1) vs. 9+/-2) but not by captopril (12+/-1). In the absence of insulin, the diaphragms from captopril- or enalapril-treated rats showed a significantly higher glucose uptake than that of controls (31% and 30% vs. control group, respectively). The presence of insulin in the incubation medium did not stimulate peripheral glucose uptake in the control group but significantly increased glucose uptake in diaphragms from captopril- or enalapril-treated rats (enhancement of glucose uptake vs. control: 52% and 43%, respectively). Endothelium-intact aortic rings from control Zucker rats showed a poor relaxant response to acetylcholine (maximal relaxation of 38.4+/-4.7%). Captopril significantly improved the endothelium-dependent vascular relaxation responses to acetylcholine and the endothelium-independent relaxation to the nitric oxide donor sodium nitroprusside whereas enalapril did not modify these relaxant responses. Neither captopril nor enalapril significantly affected the vascular contractile responses to the vasoconstrictors noradrenaline or KCl. In conclusion, the angiotensin-converting enzyme inhibitors captopril and enalapril reversed insulin resistance and the associated cardiovascular complications (cardiac hypertrophy, hypertension and proteinuria) in the obese Zucker rat, an animal model of non-insulin-dependent (type II) diabetes mellitus. However, only captopril, but not enalapril, improved the impaired endothelium-dependent and independent relaxant responses in the isolated rat aorta.
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PMID:Cardiovascular effects of captopril and enalapril in obese Zucker rats. 998 6

Diabetic nephropathy is one of the major complications of insulin-dependent diabetes mellitus (IDDM), with proteinuria being the main clinical manifestation of diabetic nephropathy. Most patients who develop overt proteinuria progress to end-stage renal disease (ESRD), usually within 5 to 7 years; ESRD necessitates dialysis or renal transplantation. Although a relationship between blood pressure reduction and delaying of ESRD has been assumed for a long time, only recently has a controlled randomised clinical trial shown that the treatment of diabetic nephropathy with an ACE inhibitor can significantly delay the loss of renal function and, therefore, ESRD. Consistent with the clinical trial on which this economic evaluation was based, the costs and consequences of 2 alternatives were considered: (i) patients subject to blood pressure control with only antihypertensive medication, but without an ACE inhibitor (placebo group) and (ii) patients given ACE inhibitor therapy (captopril group) with similar blood pressure control to the placebo group. This cost-effectiveness analysis was performed from the perspective of the Italian National Health Service [Servizio Sanitario Nazionale (SSN)]. Accordingly, only direct costs related to publicly funded healthcare services were included. The number of dialysis-years avoided (DYA) was the clinical end-point. A 10-year time horizon was considered for the economic evaluation. Captopril therapy was dominant, being at the same time more effective and less costly. The total cost for the captopril alternative during the 10-year period was 21,901,625 Italian lire (L; 1993 values) per patient, while total cost for the placebo alternative was L30,352,590 per patient. Compared with placebo, 20.01 DYA per 100 patients treated were estimated with captopril therapy during the trial period, equivalent to 2.4 months per patient. The robustness of this result was confirmed by sensitivity analysis: for both extremes, captopril remained dominant. This economic evaluation, requested by the Italian Ministry of Health, demonstrated savings in healthcare expenditure with the use of an ACE inhibitor in patients with proteinuria.
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PMID:Economic evaluation of ACE inhibitor treatment of nephropathy in patients with insulin-dependent diabetes mellitus in Italy. 1016 88


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