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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 insulin-induced hypoglycemia on the blood levels of catecholamines and renin activity has been studied in five patients with moderate hypertension before and after treatment for 3 - 8 months with penbutolol (PEN) 20 - 30 mg twice daily. Penbutolol caused no change in fasting blood glucose level. Insulin o.1 IU per kg body weight i.v. reduced blood glucose concentration by approximately 50 per cent after 30 - 45 min, both before and during treatment with penbutolol. Hypoglycemia prior to medication was accompanied by a marked increase in the production of adrenaline and a minor increase of noradrenaline in all five patients. During treatment the response of adrenaline to hypoglycemia was reduced in four patients and the data was inconclusive in one. Basal renin activity was rather low in three patients, within the normal range in one and relatively high in one. Before penbutolol the hypoglycemia-induced increase in catecholamine production caused no change in plasma renin activity in the three patients with low basal levels, whereas a marked increase was observed in the other two. During medication plasma renin activity remained unchanged on induction of hypoglycemia regardless of the catecholamine response. Despite the marked increase in plasma adrenaline following insulin-induced hypoglycemia, no statistically significant increase in pulse rate was recorded.
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PMID:Long term treatment of moderate hypertension with penbutolol (Hoe 893d). II. Effect on the response of plasma catecholamines and plasma renin activity to insulin-induced hypoglycemia. 0 1

Insulin-induced hypoglycemia previously has been shown to provoke a beta-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.
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PMID:Contrasting effects of hypoglycemia on plasma renin activity and cyclic adenosine 3',5'-monophosphate (cyclic AMP) in low renin and normal renin essential hypertension. 17 76

The frequency of latent disorders of glucose regulation during pheochromocytoma, is evaluated at 75% of cases. Detailed analysis of 83 cases with a diabetic state, gave the following results: insulin dependent diabetes, 37 cases. Non-insulin dependent, 14 cases. Latent diabetes, 32 cases. The characteristics of the insulin-dependent diabetes were not always suggestive. Insulin dependency was, however, unusual above a certain age. We noted loss of weight in spite of good control of the diabetes, the absence of acidosis and ketosis contrasting with rapid loss of weight. In fact, it is above all the hypertension which should lead to diagnosis. Surgical operation, cures or improves considerably the diabetic state, thus proving the symptomatic nature of this diabetes.
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PMID:[Diabetes mellitus in pheochromocytoma]. 18 6

In order to investigate the combined effects of diabetes and hypertension on the pathogenesis of cardiovascular disease, adult male and female SHR rats which develop hypertension spontaneously were given a single, 10 mg or 15 mg/100 g body wt. injection of alloxan s.c. to induce moderate or severe diabetes. Insulin was deliberately withheld. Animals were examined by autopsy daily for 7 days post-alloxan and after 4 and 8 weeks. Mortality was high--only 52% of the males survived as against 80% of the females. Most deaths occurred on Day 5 and were associated with adrenal haemorrhage and hyperplasia, thymus galnd involution, fatty liver and marked hypotension despite elevated aldosterone levels. During the first week, corticosterone levels increased significantly in the male; in females they showed little change. After 4 weeks, the severly diabetic animals became emaciated and moribund; corticosterone and aldosterone levels fell to very low levels despite adrenal hyperplasia. The beta cells of the moderately diabetic animals eventually lost their ability to secrete insulin and these animals too became cachetic and moribund with concomitant elevation of lipid, glucose and BUN levels, as well as myocardial infarction, fatty liver, and generalized hyalin arteriolo-, arterio-, and nephrosclerosis. It is suggested that the combined hormonal and metabolic alterations of diabetes and hypertension reinforced one another in these spontaneously hypertensive rats, leading to intense stimulation of the hypothalamic-pituitary-adrenal system, the exacerbation of those cardiovascular degenerative changes known to be associated with uncontrolled diabetes or hypertension, eventual impaired adrenocortical steroidogenesis, hypotension and death.
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PMID:Alloxan diabetes in spontaneously hypertensive rats: gravimetric, metabolic and histopathological alterations. 86 Nov 67

Fifty-one insulin-dependent nonobese diabetics with duration of disease from 15 to 40 yr were reassessed after 7 yr. Those presenting with clinical vascular disease, hypertension, or elevated fasting triglycerides initially were found to have a bad prognosis. Serum cholesterol fasting blood sugar, age, or duration of diabetes were not related to outcome, Acute insensitivity to intravenous insulin was correlated with presence of initial vascular disease and was significantly related to both death and clinical deterioration in either large or small vessels over the period of follow-up. Insulin sensitivity was reproducible and may be of value in predicting the progression of long-term vascular changes in the insulin-requiring diabetic.
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PMID:Factors influencing the prognosis of vascular disease in insulin-deficient diabetes of long duration: a seven-year follow-up. 116 91

In comparison with morphological changes of the placentae 58 pregnancies of class D and F-diabetics (with diabetic angiolopathy) were analysed. The incidence of toxaemia was 55%. Insulin requirement decreased some days before delivery in 8 cases (14%). The perinatal mortality rate amounted to 17%. Birth weights were found between 2500 and 3000 g in 9 cases, below 2500 g in 8 cases with signs of intrauterine growth retardation. The majority of placentae showed medium-sized to severe diabetic disturbances of maturation on an average more severe than in diabetics without angiolopathy. A "modification" or "mascing" of maturation disturbances by severe toxaemia is discussed. The antenatal retardation of fetal growth in some cases was attributed in part to the diabetic maturation disturbances of the placentae. Another cause may be the defective uteroplacental circulation caused by narrowing processes of myometrial and decidual arteries in consequence of long-term diabetes and hypertension.
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PMID:[Pregnancy of diabetic women with diabetic angiopathy. Clinical results in correlation of morphological findings on the placenta]. 121 43

The initial management of non-insulin-dependent diabetes mellitus (NIDDM) should include patient education, dietary counselling and, when feasible, individualised physical activity. It is only when such measures fail that drug therapy should be considered. Dietary management of NIDDM includes a restriction in calories, and these should be appropriately distributed as carbohydrates, lipids and proteins. Supplementation of the diet with soluble fibre and supplementation with magnesium salts if hypomagnesaemia is demonstrated, is recommended. However, supplementation with fish oils or with fish oil-derived omega-3 fatty acids is not currently recommended. Oral drug therapies used in NIDDM include sulphonylurea derivatives, which are a first-line treatment in patients who are not grossly obese, metformin, which is the treatment of choice for obese patients, and alpha-glucosidase inhibitors such as acarbose, which are used mainly to reduce postprandial blood glucose peaks. These types of drugs can be used alone or in combination. Insulin therapy may be required to achieve adequate control of blood glucose levels in some patients. In several instances, it is suggested that insulin therapy be combined with sulphonylureas (essentially when residual insulin secretion is present), with metformin, or with alpha-glucosidase inhibitors. The treatment of disorders associated with NIDDM, such as obesity, hypertension or hyperlipidaemia, requires particular attention in diabetic patients, since some drugs can adversely affect glycaemic control. Oral drugs for the treatment of NIDDM include sulphonylurea derivatives used in first-line treatment in patients who are not grossly obese, metformin, which is often the treatment of choice for obese patients and, more recently, the alpha-glucosidase inhibitors, such as acarbose, which are effective in reducing the postprandial rise in blood glucose.
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PMID:Management of non-insulin-dependent diabetes mellitus. 128 May 75

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37

Insulin resistance is a frequent phenomenon and a marker of increased risk for non-insulin-dependent diabetes mellitus (NIDDM) and atherosclerosis. According to recent estimations, not only individuals with obesity, NIDDM, and impaired glucose tolerance (IGT) but also one fourth of the "healthy" glucose tolerant and the majority of the hypertensive population are insulin resistant. Insulin resistance describes a tissue- and pathway-specific defect of glucose metabolism that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. The initial defect can be directly measured by glucose clamp and other sophisticated techniques; the clinical syndrome may be derived from a network of related variables known to be associated with reduced insulin action. Because neither clamps nor serum insulin screenings will be available on a widespread basis, early diagnosis based on clinical criteria is crucial. A new interpretation of the "thrifty" genotype hypothesis may explain why insulin resistance, which formerly apparently represented an advantage in the evolutionary selection process, is such a frequent phenomenon. Improvement of impaired insulin action as a therapeutic principle may play a future central role in an integrated lifestyle approach of primary prevention of noncommunicable diseases such as NIDDM, hypertension, and atherosclerosis.
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PMID:What is the clinical significance of insulin resistance? 128 40

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47


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