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

The association between fasting plasma insulin level and coronary heart disease (CHD) was studied in 909 non-insulin-dependent diabetic (NIDDM) patients, aged 45-64 years, and in 1,373 nondiabetic control subjects. Both diabetic and nondiabetic subjects with various manifestations of CHD had higher plasma insulin levels than did subjects free of CHD. By plasma insulin quintiles formed according to values in nondiabetic subjects, the age-adjusted prevalence of CHD defined by symptoms and/or electrocardiographic changes in diabetic men was 48.2% in quintiles I + II (lowest), 54.8% in quintiles III + IV, and 65.7% in quintile V (highest) (p = 0.006). The respective prevalences in diabetic women were 53.5%, 59.1%, and 73.3% (p = 0.004); in nondiabetic men, 28.1%, 33.7%, and 43.3%, respectively (p = 0.016); and in nondiabetic women, 28.1%, 34.9%, and 44.3%, respectively (p = 0.007). An essentially similar association was observed between plasma insulin level and definite or possible myocardial infarction (MI). In diabetic subjects, a positive association between plasma insulin level and CHD manifestations was also found when insulin strata were formed using quintile cutoff points determined separately from diabetic subjects. The association between plasma insulin level and the prevalence of CHD or MI disappeared or was weaker, especially in men, when adjustment was made for body mass index, hypertension, and triglyceride or high density lipoprotein (HDL) cholesterol level. The association between high plasma insulin level and CHD was significant in diabetic subjects with a body mass index greater than 27 kg/m2 but not in those diabetics with a body mass index less than or equal to 27 kg/m2. A significant clustering of hypertension, high triglyceride values, and low HDL cholesterol levels was observed in diabetic subjects in the highest insulin quintiles. The results suggest that hyperinsulinemia is an indicator of CHD in both NIDDM patients and nondiabetic subjects. Hyperinsulinemia may be directly atherogenic, but it is more probable that hyperinsulinemia reflects insulin resistance, which may be a factor enhancing atherogenesis by causing adverse changes in many CHD risk factors.
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PMID:High fasting plasma insulin is an indicator of coronary heart disease in non-insulin-dependent diabetic patients and nondiabetic subjects. 198 7

A review of continuous ambulatory peritoneal dialysis (CAPD) performed at one facility over a period of 10 years showed that age and type II diabetes mellitus were associated with the worst technique survival. The median survival of patients entering CAPD was not significantly different when the etiology of renal failure was chronic glomerulonephritis (CGN; 27 months), chronic interstitial nephritis (CIN; 21 months), diabetes mellitus type I (21 months), or hypertension (16 months). Patients with diabetes mellitus type II had significantly (P less than 0.05) worse survival (11 months). A patient remaining on CAPD 6 months had a 55% to 60% chance of remaining on therapy at 2 years and a 47% chance at the end of 3 years, whereas a patient with diabetes mellitus type II had a 34% conditional probability of remaining on dialysis at 2 years and 18% at 3 years. Sex, race, and educational achievement were not important determinants of dialysis technique survival. Studies are indicated to identify predictors of a poor dialysis experience.
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PMID:Continuous ambulatory peritoneal dialysis: ten years at one facility. 199 57

Hypertension in insulin resistance states is generally attributed to hyperinsulinemia, with resulting increases in renal sodium retention and/or sympathetic nervous system activity. However, recent data from our laboratory suggest that cellular insulin resistance, rather than hyperinsulinemia per se, may lead to hypertension. The basic tenet proposed in this review is that the common mechanism involved in the development of hypertension in both type I and type II diabetes mellitus is a deficiency of insulin at the cellular level. Recent observations suggest that impaired cellular response to insulin predisposes to increased vascular smooth muscle (VSM) tone (the hallmark of hypertension in the diabetic state). For example, recently reported studies from our laboratory demonstrate that insulin in physiological doses attenuates the vascular contractile response to phenylephrine, serotonin, and potassium chloride. Thus, insulin appears to normally modulate (attenuate) VSM contractile responses to vasoactive factors, and insulin resistance should accordingly be associated with enhanced vascular reactivity. Abnormal VSM cell calcium [Ca2+]i homeostasis may be the nexus between insulin resistance and increased VSM tone. The genetically obese, hyperinsulinemic, insulin-resistant Zucker rat demonstrates increased vascular reactivity, reduced membrane Ca2(+)-ATPase activity, increased cellular Ca2+ levels, and a marked impairment in vascular smooth muscle Ca2+ efflux compared to lean controls. Insulin stimulates membrane Ca-ATPase, blocks Ca2+ currents, and Ca2(+)-driven action potentials. Thus, an insulin-resistant state as exists in the Zucker rat may be associated with increased Ca2+ influx through voltage-dependent sarcolemmal Ca2+ channels and/or decreased production or activation of the VSM cell Ca-ATPase pump.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of hypertension in diabetes. 202 49

Insulin resistance was evaluated in 807 middle-aged subjects at a health survey, with use of an index measured in 75 g oral glucose tolerance tests. The mean value of insulin resistance was higher in a hypertensive group than among the normotensives, independent of body mass index, physical activity, smoking sex, age, and thiazide treatment. One-third of the hypertensives had a high resistance value. Another third of the hypertensives, and also about one-third of the normotensives, had a slightly increased resistance. The remaining third of the hypertensives had a normal-low resistance. A high resistance was also independently related to obesity, low physical leisure time activity, and a family history of NIDDM, but not to a family history of hypertension. The statistical analysis implied a sequence of events: low physical activity might cause high resistance, which in turn might cause high blood pressure.
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PMID:Insulin resistance in the oral glucose tolerance test--a link with hypertension. 204 30

Epidemiological evidence suggests that there is a close association between obesity, non-insulin-dependent diabetes (NIDDM) and hypertension. Obesity and NIDDM are the classical insulin-resistant states. Even in the absence of these conditions, essential hypertension is associated with insulin resistance. In view of the acute effects of insulin on renal sodium reabsorption, the sympathetic nervous system, the renin-angiotensin-aldosterone system, the transmembranous cation transport, the cardiovascular reactivity, the atrial natriuretic peptide and the kallikrein-kinin system, hyperinsulinaemia may contribute to the development of hypertension in these diseases. Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. However, extrapolation of the epidemiological data and results of acute experiments indicate that the impact on blood pressure is rather small. The pathophysiological mechanisms of hypertension in the above-mentioned conditions are also not always consistent with insulin action(s). Moreover, some data suggest that insulin resistance, and not hyperinsulinaemia per se, underlies the blood pressure elevation, while the possibility cannot be excluded that both hypertension and insulin resistance are co-inherited, but unrelated, abnormalities.
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PMID:Insulin and blood pressure regulation. 204 23

Diabetes mellitus and hypertension constitute two powerful independent risk factors for cardiovascular, renal and atherosclerotic disease. The frequent occurrence of the two diseases in the same individual doubles the risk of cardiovascular death, as well as substantially increasing the frequency of transient ischemic attacks, strokes, peripheral vascular disease with lower extremity amputations, as well as end-stage renal disease and blindness. Although hypertension usually occurs in IDDM in association with renal disease, in NIDDM the evolution of hypertension appears to be multifactorial and independent of renal disease. Obesity appears to be dissociable from hypertension and NIDDM with a common link between obesity, hypertension and NIDDM appearing to be hyperinsulinism and insulin resistance. It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Further, insulin itself may have a direct effect upon the atherosclerotic process in the hypertensive diabetic patient. These considerations have been taken into account in the structuring of antihypertensive therapy in Type I and Type II Diabetes Mellitus.
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PMID:Diabetes and hypertension. 207 56

Paraplegia is a fearful and not uncommon complication of aortic clamping in surgical procedures involving thoracic and abdominal aorta. We report a case of transient spinal cord ischemia during the early postoperative period of aortobifemoral bypass in a 69-year-old male with arteriosclerosis obliterans, hypertension, type II diabetes mellitus and COLD. The anesthetic procedure was combined (peridural + intubation and mechanical ventilation + isofluorane). Two hypotensive episodes of about 80 mmHg developed, one after induction and another in the Reanimation area. The first one had a short duration, whereas the second one required the administration of colloids, crystalloids and blood. The infrarenal aortic clamping time was 35 minutes. In the early postoperative period the patient had clinical features consistent with spinal ischemia, which progressively recovered. To prevent spinal ischemia during surgery a shorter duration than 30 minutes of aortic clamping, a higher distal perfusion pressures higher than 60 mmHg during clamping, and the attempt to exclude the least possible number of intercostal and/or lumbar vessels are recommended. Drugs (corticosteroids, naloxone) and hypothermia can be useful.
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PMID:[Spinal cord ischemia in the postoperative period of aortic surgery]. 207 98

The responsiveness of renin-angiotensin and kallikrein-kinin systems to furosemide challenge has been investigated in forty-six diabetic patients (34 NIDDM/12 IDDM), subdivided into Group I (uncomplicated DM), Group II (DM with hypertension), Group III (DM with nephropathy), Group IV (DM with hypertension and nephropathy) and a control group of 10 healthy volunteers. Plasma renin activity (PRA) was estimated by radioimmunoassay in blood samples drawn before and 10 min after furosemide administration (0.5 mg/kg i.v.). Urinary kallikrein levels were measured by bioassay using estrogenized rat uterus preparation in 4h urine samples collected before and after the diuretic. Urinary Na+ and K+ were also measured. The basal PRA in diabetics was not significantly different from controls, whereas, urinary kallikrein levels were markedly low in all patients. Both PRA and kallikrein levels increased after furosemide in controls while in diabetics this response was severely blunted. In a subset of Group I, a paradoxical fall in PRA and kallikrein levels was noted after furosemide, an effect similar to that observed in patients with nephropathy (Group III). This response in absence of clinical and biochemical parameters of nephropathy indicates early derangement of renal hemodynamic mechanisms heralding the onset of nephropathy.
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PMID:Plasma renin activity and urinary kallikrein excretion in response to intravenous furosemide in diabetic patients. 208 34

A common mechanism which may be involved in the development of hypertension in both type I and type II diabetes mellitus is a deficiency of insulin at the cellular level. Observations from a number of laboratories suggest that impaired cellular response to insulin rather than hyperinsulinemia predisposes to increased vascular smooth muscle tone (the hallmark of hypertension in the diabetic state). This review presents some of the data which suggest that there is a relationship between impaired cellular action of insulin, altered cellular calcium metabolism and the development of hypertension.
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PMID:Insulin resistance and hypertension. 209 May 12

We have studied the long term effects of captopril therapy on proteinuria in ten patients with non-insulin-dependent diabetes mellitus with hypertension and nephropathy. There were 7 males and 3 females, with a mean age of 53.3 +/- 10.6 years. After a run-in period of two weeks, therapy with captopril was started. The following parameters were studied: serum glucose, sodium, potassium, cholesterol and triglycerides, glycosylated haemoglobin, renal function and 24 hour urine protein excretion before and at six month intervals for up to 24 months. Average BP fell significantly from 182.5 +/- 28/95 +/- 7.1 to 146 +/- 16.7/76 +/- 18.1 mmHg although no significant changes were seen in the biochemical parameters studied, except a reduction in 24 hour urine protein excretion from 3.86 +/- 2.85 to 0.88 +/- 1.08 g/24 h after 24 months of treatment (P less than 0.01). No correlation was observed between the reduction in proteinuria and any other parameters studied. Our results confirm the reduction of proteinuria in patients with type II diabetes mellitus and stable diabetic nephropathy treated with captopril. This effect was maintained for a period of 24 months.
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PMID:Long term follow-up of the effect of captopril on severe proteinuria in hypertensive diabetic patients. 209 9


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