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

The effect of essential hypertension at baseline on the development of NIDDM within 6 years was investigated in 465 Chinese nondiabetics with or without hypertension. The age, sex adjusted 6 year incidence of NIDDM in hypertensive group (BP > 18.7 +/- 12. okPa (140/90 mmHg) or treated with antihypertensives) at baseline was significantly higher than that in normotensive group (44.6%, n = 325, P < 0.05) at baseline. Multivariate regression analysis showed the hypertensive group had higher risk of worsening to diabetes compared with normotensives (OR: 1.82, 95% Ci: 1.03-3.21, P < 0.05) after the adjustment for two other important risk factors for NIDDM, the fasting plasma glucose and BMI. Further more the increasement of SBP by 20 mmHg at baseline significantly increase the risk for NIDDM in the followup period in the blood-lowering-drug-free group (OR: 1.54, 95% Ci: 1.05-2.24, P < 0.05). Thus it confirmed that hypertension at baseline was an independent predictor for NIDDM. In addition, our observation showed that some antihypertensive drugs appears also to play an unfavorable role in the occurrence of NIDDM.
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PMID:[Essential hypertension: a predictor of the 6 year-incidence of NIDDM in 465 non-diabetics]. 771 8

The hypothesis of insulin resistance in the pathogenesis of arterial hypertension as part of the hormonal metabolic X syndrome and our 5H syndrome resp. (association of hyperinzulinism with hyperglycaemia-NIDDM-hyperlipoproteinaemia, hypertension and a hyperandrogenic state in women) is based on sympathomimetic, sodium retention and trophic effects of insulin. In the submitted paper the authors review opinions supporting and refuting the validity of this hypothesis. Based on the results of different studies in recent years another genetic predisposition comes also to the foreground, i.e. reduced vascularization of the skeletal muscles which on the background of insulin resistance leads to enhanced development of hypertension with subsequent hypertrophy of the vascular wall and left ventricle and to the development of arteriosclerosis. From the clinical aspect this stimulating pathogenetic concept within the framework of the hormonal and metabolic X syndrome and 5H syndrome makes it possible to use a more adequate approach to prevention and treatment not only of arterial hypertension but also of associated phenomena which enhance the risk of cardiovascular morbidity and mortality in the population. The authors summarize factors which during non-pharmacological treatment promote insulin resistance and those which improve it. When drugs are selected for pharmacological treatment, priority is given to those which improve the insulin sensitivity index (ACE-inhibitors, alpha blockers) or are at least neutral in this respect (Ca antagonists, beta blockers with ISA and cardioselective). The drugs must not enhance associated hyperlipoproteinaemia, hypercoagulability, hyperviscosity, hyperuricaemia) and they should exert a positive effect on the regression of hypertrophic vascular walls and the left ventricle.
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PMID:[Insulin resistance and arterial hypertension]. 772 34

The authors examined a group of 22 patients with significant stenoses revealed on coronarographic examination. None of the patients were diabetic. Hyperinsulinaemia was found in 12 patients (54.5%). The hyperinsulinaemic and normoinsulinaemic groups differed significantly as to the type of obesity expressed by the W/H ratio, the incidence of hypertension and triglyceride levels. The authors discuss the direct participation of insulin resistance and compensatory hyperinsulinism in the pathogenesis of atherosclerosis and its participation in the manifestation of associated risk factors (dyslipidaemia, hypertension, obesity and NIDDM).
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PMID:[Ischemic heart disease with significant coronary stenosis and insulin resistance]. 772 35

The author summarizes mechanisms by which insulin resistance and compensatory hyperinsulinism are manifested in the clinical picture. He divides the mechanisms into prereceptor, receptor and postreceptor mechanisms. The latter dominate in the population quantitatively and thus also by their impact because they create the so-called 5H syndrome (association of hyperinsulinism with hyperglycaemia (NIDDM), hyperlipoproteinaemia, hypertension, hirsutism and the polycystic ovary syndrome) or the so-called hormonal metabolic syndrome X, lethal tetrad, metabolic syndrome, syndrome of insulin resistance). The term syndrome X does not appear suitable as it is frequently mistaken for coronary X syndrome which probably is also conditioned by hyperinsulinism, for the hormonal metabolic X syndrome and probably also fot the "fragile X syndrome" in genetics. The 5H syndrome is caused by a postreceptor disorder of insulin efficiency for which so far the molecular basis and dominating organ site have not yet been defined adequately. Hyperinsulinism is conceived as an insulin resistance compensating phenomenon. In its development participates, however, in addition to compensatory hypersecretion also impaired insulin utilization (liver, muscles) and an impaired primary secretory response caused probably by a disorder of blood sugar control (glucokinase, GLUT 2). This is suggested by the frequently inadequate response of the blood sugar level, IRI and C-peptide during the oral glucose tolerance test (OGGT). A hyperinsulinaemic response may be encountered when the blood sugar curve is normal, flat, in impaired glucose tolerance and in diabetes. Thus OGGT alone is not suited for the early detection of the 5H syndrome unless concurrently the IRI and C-peptide response is recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical manifestations of the insulin resistance syndrome. The hormonal-metabolic syndrome X, the 5H syndrome and their etiopathogenesis]. 772 46

Non-insulin-dependent (type 2) diabetes mellitus (NIDDM) affects middle-aged or elderly people who frequently have several other concomitant diseases, especially obesity, hypertension, dyslipidaemias, coronary insufficiency, heart failure and arthropathies. Thus, polymedication is the rule in this population, and the risk of drug interactions is important, particularly in elderly patients. The present review is restricted to the interactions of other drugs with antihyperglycaemic compounds, and will not consider the mirror image, i.e. the interactions of antihyperglycaemic agents with other drugs. Oral antihyperglycaemic agents include sulphonylureas, biguanides--essentially metformin since the withdrawn of phenformin and buformin--and alpha-glucosidase inhibitors, acarbose being the only representative on the market. These drugs can be used alone or in combination to obtain better metabolic control, sometimes with insulin. Drug interactions with antihyperglycaemic agents can be divided into pharmacokinetic and pharmacodynamic interactions. Most pharmacokinetic studies concern sulphonylureas, whose action may be enhanced by numerous other drugs, thus increasing the risk of hypoglycaemia. Such an effect may result essentially from protein binding displacement, inhibition of hepatic metabolism and reduction of renal clearance. Reduction of the hypoglycaemic activity of sulphonylureas due to pharmacokinetic interactions with other drugs appears to be much less frequent. Drug interactions leading to an increase in plasma metformin concentrations, mainly by reducing the renal excretion or the hepatic metabolism of the biguanide, should be avoided to limit the risk of hyperlactaemia. Owing to its mode of action, pharmacokinetic interferences with acarbose are limited to the gastrointestinal tract, but have not been extensively studied yet. Pharmacodynamic interactions are quite numerous and may result in a potentiation of the hypoglycaemic action or, conversely, in a deterioration of blood glucose control. Such interactions may be observed whatever the type of antidiabetic treatment. They result from the intrinsic properties of the coprescribed drug on insulin secretion and action, or on a key step of carbohydrate metabolism. Finally, a combination of 2 to 3 antihyperglycaemic agents is common for treating patients with NIDDM to benefit from the synergistic effect of compounds acting on different sites of carbohydrate metabolism. Possible pharmacokinetic interactions between alpha-glucosidase inhibitors and classical antidiabetic oral agents should be better studied in the diabetic population.
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PMID:Antihyperglycaemic agents. Drug interactions of clinical importance. 774 82

We evaluated the course of diabetes and nephropathy in the SHR/N-cp (corpulent) rat characterized by genetic obesity, non-insulin-dependent diabetes (NIDDM), and hypertension, and examined whether the nephropathy in this model is influenced by the type of carbohydrate intake. Two groups of obese and lean SHR/N-cp rats were fed diets containing 54% carbohydrate, as either sucrose or starch for 3 months (group I) and 9 months (group II). After 3 months on either diet, group I obese rats had higher 2-h response serum glucose levels and urinary glucose excretion than lean rats. Sucrose feeding was associated with greater proteinuria and a higher percentage of abnormal glomeruli in obese rats. Morphometric evaluation of glomeruli (by computerized image analysis) showed greater mean renal corpuscular volume and mesangial fraction in obese than in lean rats fed similar diets. Mean renal corpuscular volume and mesangial fraction were also greater in sucrose-fed obese rats than in starch-fed obese rats. After 9 months, group II obese rats had substantial reductions in serum and urine glucose levels but they were still hyperinsulinaemic and showed more proteinuria than lean rats and a higher percentage of sclerotic glomeruli compared with group I obese rats. At this time, mean mesangial fraction but not renal corpuscular volume was still higher in obese than in lean rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic glomerulopathy in the SHR/N-corpulent rat: role of dietary carbohydrate in a model of NIDDM. 774 27

Gastric inhibitory polypeptide (GIP) is one of the strongest insulinotropic gut factors. Its secretion is induced by oral (but not intravenous) glucose and it has been implicated in the pathogenesis of hyperinsulinemic states (NIDDM, obesity). To determine its relevance to hypertension, 54 subjects were studied: 26 normotensives (12 with and 14 without family history of essential hypertension), and 28 essential hypertensive subjects. Plasma glucose, serum insulin (IRI), and GIP were evaluated after a mixed meal containing a total of 82 g of carbohydrates, and 2 g sodium chloride. Venous blood was collected at baseline and every 15 min during a 3-h period. Baseline levels of glucose, IRI, and GIP were comparable in the three groups. At 30 min, however, IRI and GIP were higher in normotensives with a family history of hypertension and in established hypertensive versus control subjects. Both in normotensive and in hypertensive groups, glucose, IRI, and GIP responses to the meal were significantly correlated. Our data suggest the contribution of altered GIP secretion in the pathogenesis of hyperinsulinemia in essential hypertension.
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PMID:Hyperinsulinemia and hypertension. Do intestinal hormones play a role? 775 55

Mortality from coronary heart disease (CHD) and cerebrovascular disease (CVD), as well as associated risk factors, were examined. The subjects studied were 1939 non-insulin-dependent diabetic (NIDDM) patients and 503 deaths were observed during a mean follow-up period of 9.4 years. Of these deaths, 62 were CHD deaths and 84 were CVD deaths. The mortality rates per 1000 person-years from CHD were 3.95 for males and 2.57 for females and those from CVD were 5.12 and 3.86 for males and females, respectively, showing a higher mortality for males and an increasing trend with age. The baseline factors associated with CHD mortality were age at entry into the study, hypertension, ischemic ECG changes, serum cholesterol level, diabetic retinopathy and albuminuria, while those associated with CVD were age at entry, hypertension, ischemic ECG changes, diabetic retinopathy, albuminuria and therapeutic regimen, all of which were found to be significant by univariate analysis. The relationships were further analyzed by the multiple logistic method. In addition, the baseline characteristics of the patients who died of CHD and CVD were compared with those of patients who died from other causes. The baseline characteristics in cases of deaths from CHD and CVD were significantly different from those of deaths from other causes in terms of obesity, ischemic ECG changes, serum cholesterol level and serum triglycerides level for deaths from CHD and in terms of age at onset, age at death and hypertension for deaths from CVD.
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PMID:Mortality from coronary heart disease and cerebrovascular disease and associated risk factors in diabetic patients in Osaka District, Japan. 778 97

The determinants of left ventricular mass in normal control subjects and subjects with non-insulin-dependent diabetes (NIDDM) are ill-defined. We therefore recorded M-mode and pulsed Doppler echocardiograms and 24-h ambulatory blood pressure in 57 normotensive subjects, 34 with NIDDM and 23 matched non-diabetic control subjects. Measurements of erythrocyte sodium-lithium counter-transport, plasma angiotensin II, plasma and platelet catecholamines and fasting plasma insulin were also made. Six control subjects (26%) and 15 diabetic subjects (44%) had some degree of left ventricular hypertrophy. Subjects with left ventricular hypertrophy (n = 21) had an elevated mean rate of sodium-lithium countertransport (0.40 +/- 0.13 vs 0.31 +/- 0.09 mmol.l-1.h-1; p < 0.01), parallel differences being observed in both the diabetic and control groups. Twelve of the subjects with left ventricular hypertrophy (57%) had elevated rates of sodium-lithium counter-transport compared to only seven (19%) of those without (p < 0.05). There was no consistent difference between those with and without left ventricular hypertrophy in any other clinical or biochemical variable. Multivariate analysis, with the presence or absence of left ventricular hypertrophy as the dependent variable, demonstrated that the maximal rate of sodium-lithium countertransport was the only variable that independently contributed to left ventricular hypertrophy (partial r = 0.35; F1.55 = 7.74; p = 0.007). This study demonstrates for the first time an association between left ventricular hypertrophy and erythrocyte membrane cation transport that is independent of hypertension, is present in both diabetic and non-diabetic groups, and may represent a link between elevated rates of membrane sodium transport and cardiovascular risk.
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PMID:Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM. 779 86

Insulin resistance and hyperinsulinemia are characteristic features not only of obesity and NIDDM, but are associated with the development of hypertension, hyperlipidemia, and atherosclerosis. DeFronzo et al has used the analogy that insulin resistance can be viewed as a large iceberg submerged just below the water. The physician recognizes only the tips of the iceberg--obesity, diabetes, hypertension, hypertriglyceridemia and low-HDL cholesterol, and atherosclerosis--which protrude above the surface, while the complete insulin-resistance syndrome may be missed. With the recognition that insulin resistance consists of a cluster of nutritional causes and biochemical abnormalities, it is important for the various subspecialties to work together closely to define the mechanism(s) responsible for the defects in insulin-mediated glucose metabolism and to discover effective strategies for prevention and treatment.
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PMID:Diabesity: the deadly pentad disease. 785 Dec 30


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