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

When pathophysiological and pathogenetic aspects of hypertension are taken into consideration with special regard to diabetes mellitus the exhaustion of the "insulin enhancement" within the cerebrovisceral functional systems (Baumann) are discussed and the authors enter possible connections of diabetes mellitus to the renin-angiotensin-aldosterone system. After explanation of the diabetogenic and antidiabetogenic pharmacodynamic qualities of the antihypertensive drugs adequate therapeutic recommendations are proposed summarized in a figure. The authors conclude that for the present antihypertensive therapy in diabetics taking into consideration the references reported on there are sufficient possibilities of treatment for all degrees of severity of hypertension. Such preparations as Rausedan, Disotat, Dopegyt appear as particularly suitable; moreover, the beta receptor blockers, Haemiton, Depressan as well as Guanitil and Pargylin prove to be possible or without disadvantage, respectively. Especially when diuretics are described an exact control of the metabolism should be carried out.
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PMID:[Treatment of hypertonus in diabetes mellitus]. 0 29

Four patients with idiopathic orthostatic hypotension (I.O.H.) and one with postural hypotension and diabetes were studied. Plasma-renin activity (P.R.A.) was low and did not rise appropriately with salt restriction and diuretic stimulation. Aldosterone levels were normal and rose with diuretic therapy. Plasma-volume, plasma dopamine beta-hydroxylase, urinary catecholamines, metanephrines, and vanillyl mandelic acid (V.M.A) were normal. Treatment with indomethacin (75-150 mg/day) raised the upright blood-pressure (B.P.) by an average of 20-30 mm Hg diastolic and allowed the four patients with I.O.H. to walk about without orthostatic symptoms but it had no effect in the fifth patient. When indomethacin was discontinued in one patient who had been taking it for 9 months with symptomatic relief, the B.P. fell to pretreatment levels within 48 h. When indomethacin was reinstituted the B.P. rose again. Indomethacin was more effective in these patients than either propranolol or fludrocortisone. There may be an absolute or relative excess of certain vasodepressor prostaglandins in the peripheral vessels which results in pooling of blood and orthostatic hypotension. If this is the case indomethacin might improve the orthostatic symptoms of I.O.H. by its inhibitory effect on prostaglandin synthesis, but its mechanism of action remains to be determined.
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PMID:Treatment of idiopathic orthostatic hypotension (Shy-Drager syndrome) with indomethacin. 7 34

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
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PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

Renin activity and aldosterone were evaluated relative to potassium levels and lead intoxication in 33 patients with a history of "moonshine" ingestion. Patients were divided into three groups: I, lead intoxicated with hyperkalemia; II, lead intoxicated without hyperkalemia; and III, not lead intoxicated without hyperkalemia. Those in group I demonstrated suppressed plasma renin activity, baseline and after furosemide, and blunted aldosterone responsiveness to furosemide. Plasma renin activity was not different in groups II and III, whereas aldosterone responsiveness was less in group II than in III. Group I patients tended to be older, had lower creatinine clearances, and six of nine had mild hyperchloremic acidosis. Diabetes and cortisol insufficiency were not present. Chronic lead intoxication due to illicit alcohol ingestion is associated with hyporeninemic hypoaldosteronism and hyperkalemia which appear to develop as the lead nephropathy progresses with duration and/or aging.
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PMID:Renin aldosterone system and potassium levels in chronic lead intoxication. 10 94

To determine the cause of selective aldosterone deficiency in two patients with diabetes mellitus, studies of renin and of aldosterone-precursor metabolites were performed under conditions of sodium depletion and ACTH stimulation. Plasma renin concentration was elevated in both patients, and stimulated plasma renin activity was low in one and normal in the other. Fractionation of plasma extracts demonstrated the presence of "big renin," a relatively inactive precursor of renin. Metabolites of aldosterone precursors were increased, suggesting deficient 18-hydroxylase in one patient and dehydrogenase in the other. The results suggest that hypoaldosteronism in diabetic patients may result from combined defects in both renin and aldosterone biosynthesis.
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PMID:Big renin and biosynthetic defect of aldosterone in diabetes mellitus. 18 84

In three patients with diabetes and hyporeninemic hypoaldosteronism changes in renin activity, plasma aldosterone and cortisol were examined under various conditions: orthostasis and intravenous furosemide, infusion of synthetic beta1-24 ACTH on two consecutive days and diurnal variations in basal hormone fluctuations. Each patient showed unmeasurably low renin activity unresponsive to orthostasis and intravenous furosemide while plasma aldosterone was below normal range. Under ACTH-infusion only marked increases in aldosterone were observed in one patient whereas cortisol responded normally in all diabetics tested. Analysis of diurnal night day fluctuations (20.00-8.00) in plasma aldosterone and cortisol revealed a close and statistically significant relationship between both hormones in each of the three patients (p less then 0.05-less than 0.001). Variations in plasma aldosterone thus were mediated through changes in endogenous pituitary ACTH. Compared with normal controls however, diurnal aldosterone curves were set at a lower level. Our results demonstrate that a reduced sensitivity of the adrenal gland to ACTH is not responsible for the observed subnormal plasma aldosterone levels in these patients. Therefore, the lack of circulating angiotensin II seems to be the causative reason of hypoaldosteronism. The exact mechanism of undetectable renin activity in these patients remains unknown.
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PMID:Control of plasma aldosterone in diabetic patients with hyporeninemic hypoaldosteronism. 20 28

Potassium homeostasis was evaluated in 13 patients with diabetes mellitus. In eight, plasma renin activity was low; plasma aldosterone concentration was decreased in all; seven had a history of spontaneous hyperkalemia. After administration of glucose orally, there were paradoxical increases in serum potassium levels in seven patients. After potassium loading, maximal values and increments of serum potassium were higher and fractional potassium excretion was lower in the diabetic than in the control subjects, although the differences were not statistically significant. Abnormalities of potassium homeostasis in diabetes are probably related to insulin and mineralocorticoid deficiency. Diabetic patients with hypoaldosteronism have the potential for severe hyperkalemia should renal or extrarenal mechanisms for potassium homeostasis be challenged by severe acidosis be challenged by severe acidosis, diminished renal function, marked hyperglycemia, or administration of potassium salts or potassium-sparing diuretics.
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PMID:Potassium homeostasis in chronic diabetes mellitus. 32 62

The effect of a chronic glucose osmotic diuresis on electrolyte homeostasis was evaluated in alloxan diabetic rats with urine volumes greater than 150 ml/day and glycosuria of 4 to 10 gm/day. Results were compared with control rats for periods up to 84 days. Sodium and potassium intake and urinary losses were significantly higher in diabetic animals throughout the study periods. Negative Na balance, however, persisted for only four days, and negative K balance for only 18 days. Blood volumes were elevated probably secondary to the osmotic effect of hyperglycemia (serum glucose greater than 600 mg %). Plasma renin activity decreased progressively, in part because of an early decrease in renin substrate at a time when renin concentration was normal. Despite hyperkalemia, mean plasma aldosterone was not increased compared with that in control rats, suggesting diabetic rats had relative hypoaldosteronism. Although three diabetic rats became hypertensive, no significant difference in mean blood pressure was observed between the groups. The results suggest that diabetic rats have losses of Na and K early in their diabetes, following which mechanisms to conserve Na and K are activated preventing further electrolyte depletion despite continuation of the osmotic diuresis. Decreased renin activity with inadequate stimulation of aldosterone would contribute to K conservation. Maintenance of Na balance must be explained by increased Na intake and other renal Na conserving mechanisms.
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PMID:Renin-angiotensin-aldosterone system, electrolyte homeostasis and blood pressure in alloxan diabetes. 45 34

Patients with diabetes generally exhibit normal plasma catecholamine responses to standing. Some have blunted norepinephrine responses and postural hypotension-hypoadrenergic postural hypotension due to classic diabetic adrenergic neuropathy. Others, including some with postural hypotension, have exaggerated norepinephrine responses to standing. In order to clarify the pathogenesis of this hyperadrenergic state which occurs in a subset of diabetic patients, we studied aldosterone secretion, vascular and metabolic responsiveness to the administration of norepinephrine, and intravascular volumes in four diabetic patients who were selected for their exaggerated plasma norepinephrine responses to standing. Three of the four patients also exhibited (hyperadrenergic) postural hypotension. None of the hyperadrenergic diabetic patients had evidence of hypoaldosteronism or vascular resistance to norepinephrine, but all four patients had subnormal red blood cell masses and the mean (+/-SE) red blood cell mass (13.1 +/- 1.0 ml/kg) was approximately half of that of age- and sex-matched diabetic controls (26.5 +/- 2.7 ml/kg, p less than 0.01). Thus, intravascular volume contraction, specifically a reduction in the red blood cell mass, may play an important role in the pathogenesis of hyperadrenergic state observed in a subset of diabetic patients and in the pathogenesis of hyperadrenergic postural hypotension in affected diabetic patients.
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PMID:The pathogenesis of hyperadrenergic postural hypotension in diabetic patients. 50 88

Experiments were carried out in an attempt to elucidate the mechanism of fasting-induced natriuresis in conscious rats. Female animals were given low sodium diet and saline in a fixed concentration for at least three days, and deprived of food thereafter. The sodium balance significantly shifted to negative independently of potassium supply in intact rats. Such was also observed in the dexamethasone-replaced, adrenalectomized rats and was not affected by further administration of aldosterone. In addition, the diuretic effect of insulin in fasted intact rats was not evident in the fed diabetic rats in which diabetes had been induced by streptozotocin. Such findings suggested participation of factors other than insulin. The natriuresis of fasting in intact rats appears to involve two factors, one of which is independent of the sodium intake level. Dependence on the sodium intake level may be derived from alteration of the solute diuresis-like effect of drinking saline w hen animals are fasted. These results suggest that neither aldosterone nor insulin is a major causal factor involved in fasting-induced natriuresis.
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PMID:Natriuresis of fasting in intact and adrenalectomized rats. 59 57


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