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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

To investigate the time relationships involved in cyclosporin-induced nephrotoxicity we studied changes in blood pressure, renal haemodynamics and sodium excretion in 22 adult patients with insulin-dependent diabetes mellitus treated with cyclosporin (CsA) for 4 +/- 2 days, compared to 22 insulin-dependent diabetic patients receiving conventional insulin therapy, who were matched for age and duration of diabetes. To further clarify the pathogenic role of the renin-angiotensin system, insulin-dependent diabetic patients receiving CsA were studied before and after sublingual administration of 75 mg captopril. An average of 4 days CsA treatment markedly increased blood pressure and renal vascular resistance, but did not alter glomerular filtration rate, renal plasma flow, sodium urinary excretion, or body-weight. The marked renal vasoconstriction without early changes in GFR suggests that the late decrease in GFR may involve other factors in addition to renal hypoperfusion. Acute inhibition of angiotension II formation was still able to decrease blood pressure and renal vascular resistance, although not to normal control values. These results indicate that a physiological concentration of angiotensin II may potentialise but may not be the sole factor involved in the vasopressor effect of CsA.
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PMID:Renal haemodynamic effects of short term cyclosporin A administration in patients with insulin-dependent diabetes mellitus. 211 42

Atrial natriuretic factor (ANF) may play a role in the regulation of the changes of blood volume and vascular reactivity during pregnancy and when pregnancy is complicated by hypertension. Reports of plasma ANF levels during pregnancy are conflicting. We have prospectively studied plasma ANF levels during pregnancy in 25 women, and compared these with 20 age-matched non-pregnant women. Five women developed hypertension during pregnancy and a further five who remained normotensive had insulin-dependent diabetes mellitus. Plasma ANF was 6.8 +/- 1.2 (mean +/- SEM) and 6.3 +/- 0.9 pmol/l during weeks 8-15 and 24-31 of normal pregnancy (n = 15; vs non-pregnant levels (4.0 +/- 0.6 pmol/l) P less than 0.05, n = 20). Levels were 4.3 +/- 0.8 and 3.9 +/- 0.4 pmol/l during weeks 16-23 and 32-39. In the diabetic patients and in the group who developed hypertension levels were at no time different from the uncomplicated pregnancy group. Serum aldosterone increased as pregnancy progressed, but plasma renin activity remained unchanged. As plasma ANF was not different between those who did, and those who did not develop hypertension, early measurement of it will not predict who will and who will not develop hypertension during pregnancy.
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PMID:Plasma atrial natriuretic factor levels during normal pregnancy and pregnancy complicated by diabetes mellitus and hypertension. 214 May 86

The effects of insulin treatment on plasma renin activity (PRA), plasma atrial natriuretic peptide (ANP) and body fluid volume were studied in 16 hospitalized patients with insulin-independent diabetes mellitus. Parameters were recorded for 2 days during treatment by diet alone and for 3 weeks after starting insulin. Blood samples were obtained weekly from 9 patients for the measurement of fasting plasma glucose, hematocrit, PRA and plasma ANP. A 24-hr urine sample was collected to determine the urinary excretion of glucose and sodium. In a separate group of 7 patients, plasma volume and extracellular fluid volume were determined by the Evans blue and sodium thiocyanate dilution tests, respectively. In the group of 9 diabetic patients, significant (p less than 0.05) reductions in fasting plasma glucose, hematocrit and the urinary excretion of sodium and glucose were seen with insulin treatment. PRA fell significantly (p less than 0.05) from 5.2 +/- 1.2 ng/ml/hr (mean +/- SEM) on the control days to 2.3 +/- 0.5 on the 21st day after starting treatment. Plasma levels of ANP averaged 35 +/- 5 pg/ml on the control days and these did not change significantly. In the other group of 7 patients, both plasma volume and extracellular fluid volume increased significantly (p less than 0.05) with insulin treatment. A sodium-retaining effect of insulin and a decrease in osmotic diuresis may have increased the body fluid volume and caused the fall in PRA. Thus, a vasodilatory action of insulin may assist in compensation for the increase in body fluid volume, preventing a rise in plasma ANP levels.
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PMID:Effects of insulin on plasma renin activity, plasma atrial natriuretic peptide and body fluid volume in diabetes mellitus. 214 76

The effects of streptozotocin-induced experimental diabetes on the morphology and secretory activity of the zona glomerulosa were studied in rats whose hypothalamo-hypophyseal-adrenal axes and renin-angiotensin systems had been pharmacologically interrupted by the simultaneous administration of dexamethasone-captopril and maintenance doses of ACTH-angiotensin II. The animals were examined 7, 14, 21, and 28 days after diabetes induction, which was evidenced by conspicuous hyperglycemia. Experimental diabetes caused notable atrophy of the zona glomerulosa and its cells, along with a significant decrease in both basal and angiotensin II-stimulated plasma aldosterone concentration. There was a positive linear correlation between all these changes and the number of days elapsed after streptozotocin administration. These data indicate that experimental diabetes exerts a profound time-dependent direct inhibition of rat zona glomerulosa. The hypothesis is advanced that the chronic lack of insulin that occurs in rats treated with streptozotocin, may depress de novo synthesis of structural and enzymatic proteins in zona glomerulosa cells and reduce their growth and steroidogenic machinery.
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PMID:Streptozotocin-induced experimental diabetes causes a time-dependent inhibition of growth and steroidogenic capacity of rat adrenal zona glomerulosa. 215 26

The aim of this study was to investigate the pathogenesis of hypoaldosteronism in diabetes. Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. Observations were made over 12 yr on the evolution and treatment of hyperkalemia in a diabetic subject. In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. Nine yr later, persistent hyperkalemia was documented. Upright renin activity was elevated to 5.26 ng.L-1.s-1, with concomitant elevation of 18-hydroxycorticosterone (18-OHB) and a low-normal aldosterone level. One hour after administration of 0.25 mg i.m. cosyntropin, cortisol increased normally, aldosterone increased from 220 to 360 pM, and 18-OHB increased from 3700 to 4800 pM. During treatment with fludrocortisone, fludrocortisone with furosemide, and furosemide alone, improvement of hyperkalemia was noted. Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. Evolution of hyperkalemia between 1977 and 1986 suggests this defect was acquired.
Diabetes Care 1990 Jul
PMID:Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism. 216 93

Diabetes-associated hypertension is accompanied by high levels of body sodium and cardiovascular hyper-reactivity to noradrenaline. Captopril, a promising drug for the treatment of hypertension in diabetics, may influence sodium metabolism and adrenergic pathways. This possibility was investigated in 11 patients with non-azotaemic diabetes mellitus and hypertension, studied after a 3-week placebo phase and after an 8-week phase of captopril treatment (50-100 mg/day). Blood pressure, exchangeable body sodium, blood volume, plasma renin activity, angiotensin II (Ang II), aldosterone, catecholamine levels and the pressor reactivity to infused Ang II or noradrenaline were measured. Compared with placebo, captopril caused a significant decrease in arterial pressure and stimulation of plasma renin activity. Exchangeable sodium, blood volume, plasma Ang II, aldosterone, noradrenaline and adrenaline levels, the pressor and aldosterone responsiveness to infused Ang II and the pressor response to infused noradrenaline (alone or combined with atropine) were not modified. These findings suggest that in hypertensive diabetics angiotensin converting enzyme inhibition causes a marked decrease in blood pressure. The mechanism of action is unrelated to changes in body sodium or noradrenergic-dependent pressor reactivity. In the stable phase of therapy, Ang II-dependent pathways are left unaltered when captopril is administered twice a day.
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PMID:Cardiovascular regulation during angiotensin converting enzyme inhibition with captopril in diabetes-associated hypertension. 216 58

Streptozotocin-induced diabetes significantly decreased plasma aldosterone concentration in rats whose renin-angiotensin system had been pharmacologically interrupted. Isolated zona glomerulosa cells showed a marked atrophy, coupled with a reduced basal secretion of aldosterone and corticosterone. The secretory response to the three main physiological stimuli (ACTH, angiotensin II and potassium) was also notably impaired. The hypothesis is advanced that the chronic lack of insulin may directly impair the growth and steroidogenic capacity of rat adrenal zona glomerulosa.
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PMID:Morphology and functional responses of isolated zona glomerulosa cells of streptozotocin-induced diabetic rats. 216 30

The interrelationships of sodium and volume status, atrial natriuretic peptide (ANP), plasma renin activity (PRA), insulinlike growth factor I (IGF-I), and kidney weight and their influence on glomerular filtration rate (GFR) were investigated in rats during the first 4 wk of streptozocin-induced diabetes (STZ-D). In each of three experiments, untreated diabetic rats were compared with nondiabetic control rats and rats with varying degrees of glycemic control during insulin therapy. The first experiment evaluated exchangeable sodium, plasma volume, and GFR. In untreated diabetic rats, exchangeable sodium and plasma volume, but not GFR, were increased by approximately 25% compared with control rats. Insulin-treated diabetic rats with plasma glucose levels ranging from 12 to 30 mM had increased GFR, whereas exchangeable sodium and plasma volume were reduced toward control values. Daily insulin therapy, titrated to maintain euglycemia, further reduced exchangeable sodium and plasma volume and decreased but did not normalize GFR. The second experiment evaluated the relationship between vasoactive hormones and GFR. In untreated diabetic rats, plasma ANP levels increased 89% and urinary cyclic GMP (cGMP) excretion increased 94%, with an 85% decrease in PRA, whereas GFR was unchanged. Moderate hyperglycemia (plasma glucose 12-30 mM) was associated with normalized plasma ANP levels and urinary cGMP excretion, a 52% decrease in PRA, and a 13% increase in GFR. The third experiment studied serial changes in food and water intake and vasoactive hormones and end-point measurement of kidney weight, GFR, and plasma IGF-I. In the untreated diabetic group, urinary cGMP excretion was significantly elevated after 3 wk, whereas the reduction in PRA levels was apparent after 1 wk.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1990 Oct
PMID:Glomerular filtration rate in streptozocin-induced diabetic rats. Role of exchangeable sodium, vasoactive hormones, and insulin therapy. 217 Feb 15

Black women with established essential hypertension, without renal insufficiency or diabetes mellitus, were withdrawn from their usual antihypertensive therapy for 2-3 weeks prior to entry into a study to evaluate pertinent biochemical and mineral effects of indapamide treatment. Twenty patients with a sitting diastolic blood pressure greater than 90 mm Hg had baseline measurements of plasma total cholesterol, HDL cholesterol, triglycerides, glucose, uric acid, potassium, magnesium, calcium, selenium, renin, norepinephrine, whole blood ionized calcium, and glycosylated hemoglobin. Low-density lipoprotein (LDL) cholesterol was calculated by the Friedewald equation. The patients were placed on a fixed daily dose of 2.5 mg indapamide. Blood pressure and blood tests were repeated at 4, 8, and 12 weeks of treatment. The systolic and diastolic blood pressure were both lowered significantly at week 12. Plasma renin activity was significantly increased. There was no significant change in norepinephrine, glucose, glycosylated hemoglobin, uric acid, ionized calcium, calcium, triglycerides, potassium, magnesium, or selenium. Total cholesterol increased with an increase in both high-density lipoprotein (HDL) and LDL cholesterol; however, these increases did not alter significantly either the total/HDL cholesterol or LDL/HDL cholesterol ratios. It is concluded that 2.5 mg of indapamide per day effectively lowers blood pressure with no significant adverse metabolic effects.
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PMID:Biochemical, endocrine, and mineral effects of indapamide in black women. 217 76


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