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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind, placebo-controlled study was carried out over 120 days to assess the metabolic tolerance and patient acceptability of nicardipine in 20 patients with Type 2 diabetes mellitus and slight hypertension. Following a 21-day washout period during which all patients received placebo, 13 men and 7 women (mean age 45 years, systolic blood pressure 150-165 mm Hg or diastolic blood pressure 85-100 mm Hg) were randomly assigned to treatment with oral nicardipine 60-90 mg/day (n = 9) or placebo (n = 11). No significant differences were observed between the nicardipine- and placebo-treated groups in terms of fasting and postprandial blood glucose concentrations, fasting plasma insulin levels, or glycosylated hemoglobin A1c after 60 and 120 days' treatment. There was also no change in the plasma levels of total cholesterol, HDL-cholesterol, triglycerides, and apolipoproteins. Side effects were minor and did not differ significantly between groups. All patients who had received nicardipine for 120 days wished to pursue treatment. Nicardipine, which was well tolerated, appears to be an interesting alternative for the treatment of mild essential hypertension in Type 2 diabetic patients, although further studies are required to establish its effects on renal function in this population.
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PMID:The influence of nicardipine in type 2 diabetic patients with slight hypertension. 136 5

Not all patients with diabetes develop clinically significant nephropathy and, for this reason, attention has begun to focus on the risk factors for development of this serious complication. These risk factors have not been quantified to the same degree as those factors associated with more common progressive vascular diseases, such as atherosclerosis. However, studies of pathogenesis and clinical and epidemiological surveys of diabetic nephropathy point to numerous risk categories. Glycemic control, genetic and familial predispositions, renal and glomerular enlargement, glomerular hyperfiltration, and capillary and systemic hypertension can be invoked as contributors to this disease process. This review focuses on hemodynamic alterations and their role in the development and progression of diabetic nephropathy. Increases in GFR, largely driven by increases in plasma flow and capillary pressure, appear in early IDDM and NIDDM. This abnormality of renal vascular control probably is derived from alterations in several vasoactive control systems. In addition, the elevations in capillary pressure may be damaging to the glomerular capillaries. Arterial hypertension is not necessarily present before clinical nephropathy appears; however, it is a usual concomitant of progressive diabetic renal disease. The strongest evidences for the roles of altered systemic and renal hemodynamics in the progression of diabetic renal disease are clinical and experimental studies demonstrating attenuation of the disease process by lowering systemic and capillary pressures with antihypertensive agents, and dietary and glycemic modifications. Thus, although multiple factors probably interact to determine risk for the development of diabetic nephropathy, hemodynamic forces are a particularly important contributor and are especially amenable to therapeutic intervention.
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PMID:Diabetic nephropathy. Metabolic versus hemodynamic considerations. 139 17

Information concerning cardiovascular disease risk factors in Native American children is limited. In adult Native American populations, cardiovascular disease risk factors of non-insulin dependent diabetes mellitus, obesity, and cigarette smoking are prevalent, and recent reports indicate mortality caused by cardiovascular disease has dramatically increased. In a screening program at the Onondaga Nation School, six cardiovascular disease risk factors were evaluated. Of 95 school children, 55 representing 39 interrelated families, participated. Family histories were positive for diabetes mellitus in 72%, for cardiovascular disease in 54%, and for passive smoking in 90% of families. Physical examinations of the children revealed obesity (weight/height greater than 90th percentile) in 42% and hypertension (systolic or diastolic blood pressure/height greater than 95th percentile) in 22%. Fingerstick cholesterol levels (Reflotron system) were greater than 170 mg/dL in 25%. Overall, 85% of participants had three or more risk factors for cardiovascular disease. The study results indicate that Onondaga Native American children are at significant risk for cardiovascular disease; programs for identification and modification of cardiovascular disease risk factors are urgently needed.
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PMID:Cardiovascular risk factors in Native American children. 140 96

Twenty-five middle-aged subjects with impaired glucose tolerance (IGT) were analysed 5 years later, showing normal glucose tolerance in 28% and persistent glucose deterioration in 72%. Body mass index (strongly) and 2-h glucose levels were clinically useful predictors, in the newly detected IGT-subjects, of persistent glucose deterioration (IGT or NIDDM) 5 years later. The frequency of hypertension was 36% in the newly-detected IGT subjects. Five years later this frequency increased to 54% in the persistently hyperglycaemic group, and decreased to none in the normalized group. Predictors of hypertension at the follow-up were baseline blood pressure and parts of the hyperinsulinaemic syndrome, such as serum triglyceride at baseline, BMI and 2-h glucose at the follow-up. Microalbuminuria (greater than 20 mg day-1) was not found at the 5-years follow-up, either if the subjects then had NIDDM, IGT or normal glucose tolerance. ECG abnormalities (ST segment and T wave changes) were two-fold more prevalent in the group with IGT or NIDDM than in the normalized group at the follow-up. Predictors were baseline BMI and incremental BMI. In conclusion, obesity and high 2-h glucose in newly-detected IGT-subjects seemed to predict the persistence of IGT 5 years later. Hypertension, but not microalbuminuria, was frequent when glucose deterioration persisted.
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PMID:What causes impaired glucose tolerance to deteriorate or normalize? 141 Dec 61

The traditional role of twin studies has been to assess the relative role of genetic factors as a first step in defining the genetic architecture of complex traits. This has been based on the realization that monozygotic pairs (MZ) share all their genes, while dizygotic pairs (DZ) share 50% of their genes on average. Thus, greater similarity of MZ pairs compared to DZ pairs has been taken as prima facie evidence of the role of genetic factors. This is true provided the environmental similarity of MZ pairs is not greater than for DZ pairs for effects relevant to the trait in question. This first step in genetic studies was carried out long ago in many research areas, but not in others. More detailed knowledge of the genetic architecture of traits is then obtained by other means. In this paper, we give a brief overview of some results for metabolic diseases (ischaemic heart disease, hypertension, subarachnoid haemorrhage, NIDDM and IDDM) using the classical twin approach in a large, unselected population-based twin cohort. We also outline approaches to using twins that we believe will continue to be useful, particularly for the study of environmental effects.
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PMID:Twin studies in metabolic diseases. 141 22

The effect of doxazosin, an alpha 1-adrenoceptor blocking drug, on blood pressure, sensitivity to insulin and serum lipids has been evaluated in 14 hypertensive, non-insulin dependent diabetic patients. The dose was titrated individually upwards from 1 mg until the diastolic blood pressure was below 90 mm Hg, side-effects precluded further dosage increase or the maximum daily dose of 16 mg was achieved. After 12 weeks of treatment (mean doxazosin dose 5.6 +/- 5.1 mg daily), the supine and standing diastolic blood pressure of the patients had declined by about 7 mm Hg, whereas their systolic blood pressure and heart rate were not significantly changed. The metabolic clearance rate of glucose increased from 2.35 to 3.37 ml.min-1.kg-1 during treatment, suggesting improved sensitivity to insulin. Fasting plasma glucose was 11.9 mmol.l-1 before and 10.9 mmol.l-1 after doxazosin therapy (NS). Serum electrolytes and lipids did not change significantly but serum uric acid decreased from 305 to 281 mumol.l-1. Doxazosin may be a useful alternative for the treatment of hypertension in NIDDM patients.
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PMID:Effect of doxazosin on insulin sensitivity in hypertensive non-insulin dependent diabetic patients. 145 14

The authors summarize the principles of the therapeutic approach to the 5H syndrome [1. hyperinsulinism, 2. hyperglycaemia (NIDDM), 3. hyperlipoproteinaemia (obesity), 4. hypertension, 5. hirsutism], in particular its two components, i.e. NIDDM and arterial hypertension. The authors found that early treatment of hyperinsulinism, e.g. already in the stage of impaired glucose tolerance or NIDDM with oral antidiabetics, their disproportionate increase with regard to the blood sugar level and glycosylated haemoglobin without making "hygienic" provisions (radical weight reduction; increased physical activity to the maximum possible individual level; energy restricted diet in particular as regards carbohydrates and fat) does not prevent progression of the components of the 5H syndrome to the clinical stage. In treatment of arterial hypertension associated with 5H syndrome non-selective beta-blockers and thiazide diuretics are unsuitable because they worsen the HPLP and enhance insulin resistance. Suitable preparations are combinations of ACE-inhibitors, calcium antagonists, selective beta-blockers in particular with ISA and beta-blockers with a partial selective sympathomimetic activity (devalol and celiprolol). Hygienic provisions must be started in childhood, or when hyperinsulinism is detected.
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PMID:[How should we implement the basic principles of treatment of type 2 diabetes mellitus from the aspect of the hormono-metabolic syndrome X (5H)?]. 145 53

Hypertension is a very frequent condition in individuals with non-insulin dependent diabetes mellitus (NIDDM) in Japan and has affected the occurrence of late diabetic complications, especially stroke and nephropathy. Despite similar characteristics of hypertension among Japanese and white patients, the effect of hypertension on the development of coronary artery disease (CAD) in these two populations is strikingly different. In white NIDDM patients, hypertension is one of the major risk factors for the development of CAD. However, CAD is an infrequent complication in NIDDM patients in Japan, even though they have hypertension, lipid abnormalities, and renal complications.
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PMID:Hypertension and the development of complications in patients with non-insulin dependent diabetes mellitus in Japan. 145 54

The aim of this study was to investigate the relationships among insulin resistance and albumin excretion rate in 25 nondiabetic patients with essential hypertension and in 28 patients with non-insulin dependent diabetes mellitus (NIDDM). Two groups of healthy subjects matched for age, sex, and weight served as controls. Patients with essential hypertension were divided into two subgroups: without (H1) and with (H2) microalbuminuria. Diabetic patients were divided into four subgroups: those with normoalbuminuria without (NIDDM1) and with (NIDDM2) hypertension and those with microalbuminuria without (NIDDM3) and with (NIDDM4) hypertension. Whole-body glucose utilization during euglycemic hyperinsulinemic clamp (40 mU/m2/min insulin infusion) was calculated by tracer dilution techniques (6,6 2H2 glucose tracer continuous infusion) and was significantly lower in hypertensives with microalbuminuria than in those without (H2 versus H1 versus controls: 3.41 +/- 0.51 versus 6.52 +/- 0.62 versus 7.03 +/- 0.48 mg/kg/min; mean +/- SE). Whole-body glucose utilization in NIDDM patients--NIDDM4 versus NIDDM3 versus NIDDM2 versus NIDDM1 versus controls--was: 1.86 +/- 0.31 versus 2.21 +/- 0.39 versus 2.01 +/- 0.40 versus 5.98 +/- 0.77 versus 5.52 +/- 0.92 mg/kg/min (mean +/- SE). Whereas the first three subgroups did not differ among themselves, they had significantly lower glucose utilization than did the normotensive NIDDM1 patients without microalbuminuria and nondiabetic controls (P < 0.01). Hypertensives with microalbuminuria had higher Vmax of sodium-lithium countertransport (Na/Li CTT) in red blood cells than did both hypertensives without microalbuminuria and controls. It was also observed that NIDDM patients with microalbuminuria had higher Vmax of Na/Li CTT than did NIDDM patients without microalbuminuria and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Close relationship between microalbuminuria and insulin resistance in essential hypertension and non-insulin dependent diabetes mellitus. 145 61

To assess the short-term metabolic effects a long-acting non-sulphydryl ACE-inhibitor benazepril on glycaemic control in Type 2 diabetes mellitus and arterial hypertension, 10 hypertensive diabetic patients treated with glibenclamide were studied in a double-blind, crossover fashion over two 10-day periods in which either benazepril (10 mg/day) or placebo was given. At the end of the 10 day treatment, both blood pressure and plasma glucose concentrations were lower after benazepril versus placebo (benazepril, blood pressure: 143 +/- 11/83 +/- 5 mmHg, plasma glucose: 7.1 +/- 1.2 mmol/l; placebo: blood pressure: 157 +/- 10/99 +/- 2 mmHg, plasma glucose: 8.2 +/- 1 mmol/l, p < 0.05). In response to an oral glucose tolerance test combined with 1 mg intravenous glibenclamide, plasma glucose levels were lower after benazepril versus placebo (0-460 min: 8.4 +/- 0.8 versus 10.5 +/- 0.9 mmol/l, p < 0.05), whereas plasma insulin, C-peptide and glibenclamide concentrations were not different. It is concluded that a short-term administration of benazepril in Type 2 diabetes mellitus reduces blood pressure and improves blood glucose control, most likely by decreasing insulin resistance.
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PMID:Short-term metabolic effects of the ACE-inhibitor benazepril in type 2 diabetes mellitus associated with arterial hypertension. 145 16


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