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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose intolerance and noninsulin-dependent diabetes are commonly associated with hypertension. 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. When hypertensive patients whether obese or of normal weight are compared with matched normotensive control subjects, an increased plasma insulin response to a glucose challenge is consistently observed. Studies using insulin glucose clamp techniques in combination with tracer glucose infusion and indirect calorimetry have demonstrated that the insulin resistance in hypertensive subjects is located in muscles and restricted to glycogen synthesis. The relations between hyperinsulinemia and blood pressure do not prove that the relationship is a causal one. However, at least four mechanisms may link hyperinsulinemia with hypertension: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport and proliferation of vascular smooth muscle cells. Diuretics and beta-blockers may enhance insulin resistance, which is not affected by calcium antagonists, but decreased by the ACE inhibitor captopril. Weight reduction and regular physical exercise can improve insulin sensitivity and decrease blood pressure values. These nonpharmacological interventions should be more strongly recommended to diabetic and nondiabetic hypertensive patients.
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PMID:Hyperinsulinemia, insulin resistance and essential hypertension. 130 12

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6

During the past years, several large trials (Consensus, VHEFT I and II, SOLVD) have shown a significant reduction of mortality in patients with moderate and severe heart failure. However, despite effective treatment with vasodilators, digitalis and diuretics mortality in these patients remains unacceptable high. It seems logic, to state treatment at an earlier stage of the disease to achieve more benefit. The main early pathophysiological disturbance is left ventricular hypertrophy, resulting from hypertension, coronary artery disease, increasing age and obesity. On the long run, LVH may lead to diastolic and systolic heart failure, myocardial ischemia, arrhythmias and sudden death. With ACE-inhibitors LVH can be reduced within 1 month of treatment. The large SAVE- and SOLVD-prevention trials will show, whether this early intervention will improve proposis in patients with asymptomatic heart failure.
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PMID:[Early therapeutic intervention in heart failure]. 141 67

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

The effect of the new ACE-inhibitor, fosinopril, on insulin sensitivity (SI), glucose homoeostasis and lipid profile has been examined in 24 young, healthy, normotensive men. SI, fasting plasma glucose and insulin, serum total triglycerides (Tg) and lipoprotein cholesterol (C) fractions, and ACE activity were assessed after subjects had taken placebo for 1 week and after 3 further weeks either on placebo (12 subjects) or fosinopril 20 mg daily (12 subjects), administered in a double-blind, randomized order. Measurements were made after 3 days on a standard diet (2500 kcal/d, 45% carbohydrates, 40% fat and 15% proteins) and after an overnight fast. Compared with control values at the end of the run-in placebo phase, fosinopril reduced plasma ACE activity (from 106 to 24 nmol.ml-1.min-1), Significantly increased plasma potassium and lowered upright systolic blood pressure. It also improved the k-value of the glucose disappearance rate after glucose load (from -1.70 to -1.88%.min-1) and tended to increase SI slightly although not significantly (from 10.2 to 12.0.10(-4).min-1.microU-1.ml-1). Fasting plasma glucose, insulin, serum total, high-, low-, and very-low density lipoprotein cholesterol fractions and total triglycerides were unchanged following fosinopril and placebo. The findings indicate that in healthy lean humans, ACE inhibition with fosinopril is neutral with regard to lipoprotein and carbohydrate metabolism, and that it may slightly enhance cellular glucose disposal. This calls for further evaluation in individuals at high risk of developing insulin resistance and in patients with impaired insulin sensitivity related to hypertension, obesity, decreased glucose tolerance and diabetes mellitus.
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PMID:Insulin sensitivity in normotensive subjects during angiotensin converting enzyme inhibition with fosinopril. 153 88

A rare case of ACTH-independent Cushing's syndrome due to carcinoma is described. A thirty-year-old woman presented with systolic-diastolic hypertension, unsuccessfully treated for several months with ACE and beta-blockers. During this period physical changes such as centripetal obesity, rubeosis, and hair loss were observed. Elevated urinary and plasmatic cortisol levels were essential for the diagnosis. Alterations of the circadian rhythm with higher levels in the evening compared to the morning were registered. ACTH was found to be suppressed in several tests. Ultrasound and abdominal CT scan showed a mass involving the left adrenal gland. While waiting for surgery, the patient underwent ketoconazole therapy. The operation was carried out by bilateral chest laparotomy and consisted in a left adrenalectomy with regional lymphadenectomy. At 18 months from the operation the patient is in excellent health, the classic signs of Cushing's syndrome have disappeared and laboratory tests are normal.
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PMID:[A case report of Cushing's syndrome due to an adrenal carcinoma]. 158 Nov 62

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26

The most common cause of death in hypertensive patients is myocardial infarction (MI), being three times more common than stroke. Lowering raised BP results in 40% fewer strokes, but only 14% fewer MIs. This may be because other coronary risk factors that often accompany hypertension (e.g. obesity, lipid and thrombotic disturbances, insulin insensitivity, increased plasma renin activity and increased sympathetic activity) are either unaffected or exacerbated by some of the traditional antihypertensive agents. Some of these risk factors show a diurnal rhythm peaking at 07.00-10.00 hours, thus this time constitutes a 'vulnerable period' for sudden death or death from MI. beta-blockers and diuretics have been effective in preventing stroke, but diuretics (at least potassium-losing diuretics) might actually increase the incidence of sudden death and MI in young to middle-aged hypertensive subjects (though elderly patients may benefit). Quality of life can be impaired by some beta-blockers, and diuretics can cause metabolic upset and male impotence. Thus, antihypertensive agents that are not only effective and well tolerated but are beneficial to the broader coronary risk profile are desirable. ACE inhibitors should prove particularly useful in terms of: good quality of life; non-exacerbation or improvement of coronary risk factors; treating patients with impaired left ventricular function; reversing left ventricular hypertrophy and vascular wall hypertrophy, thus improving coronary flow reserve; atheroma regression; renal protection, particularly in diabetes; and prevention or regression of LV dilatation (remodelling) following MI.
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PMID:What does the future hold for ACE inhibitors? 179 18

Overweight and obesity may develop in individuals with genetically determined low resting energy expenditure. Drugs are among the recognised precipitating factors. The obesity promoting impact of beta-blockers is, however, less well known. Resting energy expenditure, and thermogenesis induced by stimuli such as meals, cold and heat exposure, stress and anxiety, have a facultative component mediated by the sympathoadrenal system through catecholamines working on beta-adrenoceptors. Treatment with beta-blockers reduces the facultative thermogenesis by 50-100 kcal/d, which corresponds to the weight gain of 2-5 kg/year reported in clinical trials. Treatment with beta-blockers also results in insulin resistance, which may aggravate existing diabetes and elicit diabetes in predisposed patients. Overweight and obesity are frequently complicated with hypertension and angina pectoris, which are often treated with beta-blockers. Obesity is associated with a defective sympathetic activity, and treatment with beta-blockers may further reduce facultative thermogenesis and promote weight gain. The consequence may be aggravation of hypertension, insulin resistance and other atherogenic factors. The causal therapy of android overweight and obesity complicated with diabetes or hypertension is a sufficient weight loss. If pharmacological treatment is inevitable, combined treatment with diuretics and ACE-inhibitors are most appropriate.
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PMID:[Obesity and diabetes as side-effects of beta-blockers]. 197 28

Joint studies of the ALIMDA and Society of Actuaries, notably those of 1935, 1959 and 1979, established that there is a progressive rise in cardiovascular mortality with successive increments in blood pressure. This has provided the basis of underwriting. The converse is not true, or at least has not been true until very recently. Drugs that effectively reduce blood pressure have been available for several decades, but reduction and maintenance of blood pressure is still accomplished in only a minority of hypertensives. Long-term trials employing a combination of drugs, i.e., diuretics, vasodilators and reserpine and subsequently beta-blockers, almost without fail have not shown that treatment with these agents significantly reduces heart disease mortality and sudden death. This has been attributed, perhaps without basis, to an unfavorable countering effect of increased lipid levels, aggravating this risk factor, and other undesirable metabolic effect of diuretics, such as hypokalemia and depletion of body magnesium, increasing the propensity to ventricular arrhythmias, hyperglycemia, worsening diabetes, and hyperuricemia. A survey of 674 persons with hypertension seen personally during the period 1985-89, who were under the care of approximately that many physicians, reveals striking changes in drug prescription and use during this brief period that portend a major change in the outlook of hypertension. Two classes of drugs have increased rapidly in popularity: these are the angiotensin-converting enzyme inhibitors (ACE inhibitors) and the calcium blockers. Both classes of drugs effectively lower blood pressure and have minimal side effects with good compliance. They act not only to reduce peripheral vascular resistance, but also locally in the heart muscle to directly cause left ventricular hypertrophy to regress, an effect of great consequence. The drugs used in former trials such as the vasodilators and diuretics have no effect on left ventricular hypertrophy, unlike the ACE inhibitors and calcium antagonists. Left ventricular hypertrophy is the key lesion in hypertension and is only in part due to increased work load imposed by elevated pressure. It is associated with elevated blood pressure, but not closely and occurs independently; ventricular myocytes as well as myocytes of the vasculature being stimulated to growth by angiotensin and calcium, potentiating the effect of norepinephrine. Left ventricular hypertrophy greatly increases the propensity to ventricular arrhythmias and sudden death, and is a prime cause of cardiac mortality and sudden death not only in hypertension, but also in obesity, aging and diabetes, in which conditions left ventricular hypertrophy also is very common.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Major new developments affecting treatment and prognosis in hypertension. 235 5


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