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

The treatment of hypertension in patients with diabetes, obstructive airway disease, impaired renal function, or congestive heart failure (CHF) is discussed. Specifically, the value of alpha 1-adrenoceptor blocking agents in such patients is reviewed. An individualized approach to therapy is required, with careful consideration of the effects of different drugs on the existing metabolic and hemodynamic situation. In diabetic individuals, commonly used step-1 agents may impair glucose tolerance; beta-adrenergic blockade may increase blood glucose levels and significantly change response to insulin-induced hypoglycemia. Diabetic patients may also be especially sensitive to side effects of some centrally acting antihypertensive agents. In patients with obstructive airway disease, beta-blockade and alpha-stimulation worsen bronchospasm; although beta-stimulants produce bronchodilatation, they often are contraindicated in hypertensive patients due to their stimulatory effects on the heart. In patients with impaired renal function, therapy for hypertension may include problems such as an increased half-life of antihypertensive agents and retention of active metabolites. In patients with CHF, if blood pressure is not normalized with diuretics, more aggressive therapy may be required. According to results of several studies discussed, the alpha 1-adrenoceptor blocking-agent prazosin appears to be a safe and effective therapy, causing a minimum of side effects, for treatment of hypertension in patients with these conditions.
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PMID:Management of hypertension in patients with concomitant diseases. 354 75

200 years have gone by since the autonomic disturbance in diabetes mellitus has been described for the first time ever. There is a great deal of information on the close relationship between somatic and visceral symptoms in diabetic polyneuropathy (PNP), so that there should be talked about only of one form of manifestations within the meaning of a distal symmetric somatovisceral PNP. The longer fibres such as the vagal fibres of the viscus, sympathetic fibres of the eye are affected at first and more intensively in the autonomic region same as in the sensory and motor region. Due to the fact that for reasons of fragmentary knowledge pathogenetically substantiated classification of the autonomic disturbances in diabetic PNP is not at hand, such a classification is being made from organotopic and phenomenologic aspects. Frequently, afferent denervation of an organ results in enhancing the effects of an autonomic innervation dysfunction, as for instance in unnoticed hypoglycaemia, in order to modify the symptoms, as for instance in rectal incontinence with unnoticed defecation, or rather to let new symptoms appear, for instance loss of testicular pain. In recent years, appropriate methods of examinations were tested for the clinical routine, permitting to give evidence of autonomic dysfunctions before clinical manifestation. It is still unclear to what extent such subclinical abnormalities are reversible with a more favourable regulation of the metabolic process, for instance with the aid of continuous subcutaneous insulin injections. An impressive symptom of innervation dysfunctions of the cardiovascular system is orthostatic hypertension that may, in exceptional cases, even lead to confinement to bed. The most important pathogenic factor seems to be vascular denervation. A pronounced tachycardia at rest, frequently found in diabetics, is the result of the failure of the vagal autonomic system, and, after additional destruction of the sympathetic fibres, it adjusts itself to a lower level that cannot be changed by reflex mechanisms. Cardialgia absent in the case of myocardial ischemia is a factor of an increased mortality of long-term diabetics. The correlation between vascular denervation and arteriosclerosis or mediasclerosis, respectively, is being under discussion. Denervation on the gastrointestinal tract has an effect on the motility and excretory functions. The innvervation dysfunctions lead to sialadenosis by changing the composition of saliva. In most cases esophageal dysfunction is not perceived by the patient.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Autonomic symptoms in diabetic polyneuropathies]. 359 51

Functional development of the sympathetic nervous system was examined in inbred Dahl salt-sensitive (S/JR) and salt-resistant (R/JR) rats by assessing cardiac and adrenal medullary responses to insulin-induced hypoglycemia at 2, 4, 8, 12, and 16 days of age. Heart ornithine decarboxylase (ODC) activity and adrenal catecholamine content were measured in pups of the two strains 3 hours after administration of either saline or insulin. The centrally mediated increase in sympathetic outflow caused by insulin-induced hypoglycemia was attended by induction of heart ODC activity and depletion of adrenal epinephrine (EPI). No significant differences were found overall between R/JR and S/JR strains with regard to either heart ODC activity or adrenal epinephrine. This was true for basal values obtained from saline-injected pups as well as for measures from insulin-injected pups. Functional innervation of the heart was present in pups of both strains as early as 2 days of age, while in the adrenal medulla a significant response to stimulation was not detected until 8 days of age. While the susceptibility for hypertension in the salt-sensitive animals may well be linked to increased sympathetic tone, the present findings indicate that S/JR rats do not have an accelerated development or a hyperresponsiveness of sympathetic input to either the heart or the adrenal medulla during the pre-weanling period.
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PMID:Sympathetic responses of the heart and adrenal medulla in developing Dahl hypertensive rats. 360 26

The differential leukocyte count was studied within the first 24 hours of life in 115 infants of diabetic mothers (IDMs) appropriate for gestational age (AGA), 16 IDMs large for gestational age (LGA), 104 infants of non-diabetic mothers (INM's) AGA, and 22 INMs-LGA. A significant "shift to the left" was found in IDM's-LGA only. The usual cause of "shift to the left" such as maternal hypertension or fever, respiratory distress syndrome, meconium aspiration, neonatal asphyxia, sepsis, convulsions, or hypoglycemia could not explain this finding. It is hypothesized that increased glucocorticoid secretion may possibly play a role.
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PMID:Differential leukocyte count in infants of diabetic mothers. Increased band count associated with macrosomia. 373 70

The clinical usefulness of calcium antagonists was studied in four patients with reactive hypoglycemia including two with alimentary and two with idiopathic. All patients had hyperresponses of plasma insulin (IRI) and C-peptide (CPR) during an oral glucose tolerance test (OGTT). A calcium antagonist (diltiazem 90 mg/d, or nifedipine 30 mg/d, or nicardipine 60 mg/d) was administered orally for about two months. After two months of treatment, plasma IRI and CPR responses during the OGTT were clearly suppressed in all patients and symptomatic reactive hypoglycemia disappeared. One month after the discontinuation of the treatment in two patients, plasma IRI and CPR responses during the OGTT became higher again and symptomatic reactive hypoglycemia recurred. In addition, an intravenous glucose tolerance test was performed before and after two months of the treatment with calcium antagonists in the two patients with reactive hypoglycemia and seven patients with hypertension, who were free from glucose intolerance and were also treated with a calcium antagonist. In these patients, plasma IRI and CPR responses were also reduced after the treatment compared with those before the treatment. These results suggest that calcium antagonists are useful as therapeutic agents for the treatment of reactive hypoglycemia associated with hyperinsulinemia, and that one of the main mechanisms of action of calcium antagonists is a direct action on the pancreatic B-cell to inhibit glucose-induced insulin release.
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PMID:Effect of calcium antagonists on reactive hypoglycemia associated with hyperinsulinemia. 376 99

Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% +/- 0.49% with significant elevations to 81.96% +/- 0.47% and 82.95% +/- 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2-9 mmHg and the range of peak values in galactosamine-treated rabbits was 18-55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.
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PMID:Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure. 377 Mar 59

A 26-yr-old woman presented with hirsutism, male pattern scalp baldness ("geheimratsecken"), and menstrual irregularities. She had no hypertension or other signs and symptoms of Cushing's syndrome. Plasma cortisol levels were greatly elevated and did not suppress normally in response to dexamethasone. Cortisol binding to transcortin was normal. Plasma androstenedione and testosterone levels were also increased, but 17-hydroxyprogesterone and aldosterone levels were normal. Further studies revealed an increased cortisol production rate, increased 24-h urinary cortisol excretion, increased plasma ACTH levels, a normal diurnal rhythm of cortisol at an elevated level, and normal increments of plasma ACTH, cortisol, GH, and PRL in response to insulin-induced hypoglycemia. The father and two brothers also had increased plasma cortisol levels, which did not suppress normally in response to dexamethasone. Chronic therapy with dexamethasone (at first 1 and later 0.5 mg, three times daily) for more than 30 weeks resulted in decreased hirsutism, normalization of scalp hair and menstrual cyclicity, and normal plasma testosterone and androstenedione levels. No signs or symptoms of Cushing's syndrome developed, and the central regulation of secretion of ACTH, cortisol, GH, and PRL (insulin test, diurnal rhythm) remained qualitatively normal at a lower set-point. We conclude that this patient had autosomal dominantly inherited hereditary (partial) cortisol insensitivity, which had resulted in increased adrenocortical cortisol and androgen secretion. The latter had not resulted in clinical symptoms in the three afflicted male members of the family, but had in the propositus. The results also indicate the potential usefulness of the insulin test in distinguishing this disorder from Cushing's disease.
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PMID:Familial cortisol resistance: differential diagnostic and therapeutic aspects. 378 21

To evaluate the response during insulin-induced hypoglycemia, diabetics treated with relatively selective or nonselective beta-adrenergic blocking agents were studied. Placebo, atenolol (100 mg/day), and propranolol (80 mg b.i.d.) were administered to 12 insulin-treated diabetics for 1 week in a double-blind, randomized, crossover fashion with a 2-week washout between treatments. Sufficient intravenous insulin (0.2-0.6 units/kg) was administered to decrease plasma glucose 68% from the basal level or to less than 60 mg/dl within 90 minutes. Blood pressure changes at the nadir of plasma glucose were +15.2/-9.9 mm Hg for placebo, +27.9/0 mm Hg for atenolol, and +38.8/+14.3 mm Hg for propranolol. Diastolic blood pressure changes induced by propranolol were significantly different from those induced by atenolol (p less than 0.01) and placebo (p less than 0.01), and systolic pressure changes were significantly different (p less than 0.02) between propranolol and atenolol. Mild seizures developed in two patients treated with propranolol. Their blood pressure changes at the plasma glucose nadir were +56/+22 and +86/+31 mm Hg. Other symptoms of hypoglycemia were more frequent during beta-blocker than during placebo treatment. Differences in response may be related to the relatively selective adrenergic blocking effect of these drugs.
Hypertension
PMID:Hypertension in hypoglycemic diabetics treated with beta-adrenergic antagonists. 388 36

The health consequences of obesity in adults encompass both metabolic and cardiovascular complications. Pregnancy in obese women also has a particular set of problems. For the obese pregnant woman, these include weight gain less than 5.4 kg, chronic hypertension and superimposed preeclampsia, gestational diabetes, multiple gestation, and the potential for a macrosomic child. The combination of obesity and maternal diabetes does not appear to have an additive effect on the excessive growth of infants of obese mothers. Furthermore, despite inadequate weight gain, hypertension, and multiple gestation, infants of obese mothers are usually born with a greater birth weight than those of nonobese women. In addition, the incidence of intrauterine growth retardation is lower after an obese pregnancy. Neonates born to obese mothers have increased risk for birth asphyxia and birth trauma. Recently infants born to obese women were noted to have transient neonatal fasting asymptomatic hypoglycemia. Hyperinsulinism is not present in the infants of obese mothers; thus, alternate fuel mobilization (free fatty acids, glycerol, ketones) may respond to the hypoglycemic stimulus. Suggestions and rationale for the management of the pregnant obese woman, fetus, and newly born infant are discussed in the text.
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PMID:Perinatal problems of the obese mother and her infant. 389 77

In an open, controlled trial, treatment with a combination of metoprolol and hydralazine was compared with non-pharmacological management of mild and moderate hypertension in pregnancy. One hundred and sixty-one women participated in the study. The drug-treated group showed significantly better blood pressure control than the group not given antihypertensives. Induction of labor before term, because of maternal or fetal complications, was somewhat more frequent in the control group. Nine women in the treatment group and 5 in the control group developed albuminuria. Three infants in the drug-treated group died perinatally, and one in the control group. The outcome for the newborns was similar in both groups concerning birth weight, head circumference and Apgar score and in the frequencies of respiratory distress, bradycardia and hypoglycemia. The better blood pressure control achieved with these drugs makes it possible to treat the patient at home and reduce the risk of emergency delivery, but treatment does not seem to be mandatory for a good outcome of the pregnancy in cases of mild and moderate hypertension during pregnancy.
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PMID:A prospective controlled trial of metoprolol-hydralazine treatment in hypertension during pregnancy. 390 22


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