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

In a prospective, randomized, double-blind, multicentre trial the effect of antenatal treatment with betamethasone phosphate was compared with placebo in the prevention of the respiratory distress syndrome (RDS) in preterm infants. The dose of betamethasone was 4 mg every 8 h for six doses, unless delivery occurred. The 251 women who were enrolled gave birth to 262 liveborn infants, 130 in the beta-methasone and 132 in the placebo group; the two groups were evenly matched in most respects. The diagnosis of RDS in the newborn was confirmed by two independent assessors. Seven of the 130 infants in the betamethasone group and 16 of the 132 in the placebo group developed RDS. In infants whose mothers had received at least three injections, RDS was also less frequent in the steroid group than in the placebo group (3/104 and 10/104 respectively; P less than 0.05). There was a significant reduction of RDS in those born between 24 h and 6 days after entry into the trial (0/30 and 8/45 respectively; P less than 0.05). The largest difference in frequency of RDS occurred in the subgroup of infants born before 34 weeks gestation, within 8 days of trial entry, and whose mothers had received at least three injections (0/27 steroid group and 7/32 placebo group; P = 0.03), and there were also significantly fewer neonatal deaths (2/27 and 13/32, respectively; P less than 0.01) in this subgroup. Betamethasone did not provoke earlier delivery. Premature rupture of the membranes and maternal hypertension did not seem to contraindicate the use of steroids: there was no increase in maternal or neonatal sepsis nor in stillbirth in hypertensive pregnancies in the steroid group. Neonatal jaundice was significantly less frequent in the steroid (55/129) than in the placebo group (81/127; P less than 0.01) but not in the subgroups born before 34 completed weeks gestation.
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PMID:Antenatal administration of betamethasone to prevent respiratory distress syndrome in preterm infants: report of a UK multicentre trial. 266

Any type of chronic renal disease is associated with functional deterioration of the kidney due to progressive glomerulosclerosis with interstitial fibrosis and tubular atrophy. This process is thought to be predominantly due either to glomerular hyperfiltration or mesangial overload with macromolecules. Antihypertensive therapy, particularly with ACE inhibitors, and protein restriction have been found to retard progressive glomerulosclerosis in animal experiments. There is no doubt that patients with renal disease benefit from antihypertensive therapy through both preservation of renal function and prevention of secondary organ damage due to hypertension. However, the value of protein restricted diets with or without supplements of essential amino acids or ketoacids is less clear. A patient treated with protein restriction is presented and the investigations necessary to monitor compliance, renal function and nutrition are discussed. Monthly to quarterly controls of renal function, blood pressure and mineral metabolism are suggested, particularly in the case of severe hypertension and of prophylactic treatment for renal osteodystrophy with phosphate binders and vitamin D metabolites. Finally, guidelines are provided for planning of renal replacement therapy by dialysis and renal transplantation in the individual patient.
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PMID:[Long-term management of patients with chronic renal failure]. 267 34

Malignant hyperthermia (MH) is a pharmacogenetic disease in man and animals. It primarily involves skeletal muscle tissue, but other tissues might be affected to a lesser degree. Calcium homeostasis in muscle cells is upset in susceptible individuals, so that various agents and circumstances can increase the free, ionised intracellular calcium concentration to damaging levels. The primary defect is not known at present, but is believed to involve an abnormally sensitive calcium-induced calcium release mechanism. Thus small, localised increases in calcium concentration releases more calcium so that a vicious cycle is triggered. The increased calcium concentration causes multiple effects in the muscles by stimulating contraction and a hypermetabolic state, clinically observed as rigidity and fever. If demands on the homeostatic mechanisms to lower the calcium concentration become exhausted, and metabolism is insufficient to supply enough phosphocreatine and ATP, membrane potentials cannot be maintained, and permeability of the cell membranes increase. This causes loss of phosphate and H+ as well as K+ and Mg++, and later myoglobin and creatine kinase. Thereby oxidative metabolism is further impeded with formation of lactate as a result. The ensuing acidosis stimulates sympathetic innervation, resulting in tachycardia, high blood pressure, and vasoconstriction. Hyperkalemia causes arrhythmia. Dantrolene inhibits the release of calcium and can halt the process if given before depletion of the energy rich phosphates is too advanced.
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PMID:Pathophysiology of malignant hyperthermia. 269 55

18 anemic patients undergoing maintenance hemodialysis were treated with recombinant human erythropoietin (EPO) 1-3 times per week for 10.7 +/- 3 months. 4 patients underwent renal transplantation whereas 14 patients could be followed up during 12 months of EPO treatment. Hemoglobin concentration rose (from 7.0 +/- 0.7 to 11.0 +/- 1.1 g/dl, p less than 0.001) with an EPO maintenance dose of 298 units/kg/week. Blood transfusions were totally eliminated. 12 patients without iron overload required iron supplements. In the course of an infectious episode and notwithstanding an increase in EPO dosage, 2 patients exhibited a fall in hemoglobin which rose again after successful treatment of the infection. The few complications observed in connection with the rise in hemoglobin were: 1. deterioration of arterial hypertension in 7/18 with hypertensive encephalopathy in 3 patients, 2. thrombotic occlusion of the vascular hemodialysis access (a-v fistula) in 3/18, 3. periarticular inflammation with calcified deposits due to an elevated calcium-phosphorus product of 6.8 mmol/l in 4/18, 4. occurrence of hyperkalemia (6.9 +/- 0.3 mmol/l) in 7/18. These complications were more frequent during the first 3 months. They were corrected with close monitoring, drug therapy for hypertension, and intensification of dialysis and of treatment with phosphate binding substances, with the result that no differences were found in 14 patients before and after 12 months of treatment with EPO (blood pressure 133 +/- 25/77 +/- 9 vs 139 +/- 26/79 +/- 13 mm Hg [ns], potassium 5.4 +/- 0.4 vs 5.6 +/- 1.0 mmol/l [ns] and calcium-phosphorus product 4.3 +/- 1.0 vs 4.6 +/- 1.3 [ns]).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of anemia in hemodialysis patients using recombinant human erythropoietin: advantages and disadvantages]. 271 Nov 61

Anemia is an almost invariable feature of chronic renal failure and is particularly severe in children treated by long-term hemodialysis. Recombinant human erythropoietin (rhEPO) offers entirely new aspects in the treatment of renal anemia. This report presents three patients on maintenance hemodialysis aged 10, 10/10 12, and 18 years who were treated with rhEPO. Two suffered from hemochromatosis secondary to multiple transfusions. 100 U/kg rhEPO were administered three times weekly, and venesection after dialysis was performed when a target hematocrit value of 30% was achieved. Hematocrit, reticulocyte-counts and hemoglobin rose within 3 to 6 weeks after initiation of therapy in all patients. Serumferritin levels declined significantly in the two patients with hemochromatosis. No deterioration of the metabolic status (i.e. increase of blood urea nitrogen, serum-creatinine, -phosphate or -potassium) could be detected. Therapy had to be discontinued in one patient who experienced hypertensive ceisis. This patient, however, had suffered from severe hypertension prior to rhEPO therapy. Blood pressure remained stable in the other patients. We conclude that renal anemia can be effectively treated by rhEPO in children. Increase of blood pressure may necessitate discontinuation of therapy especially in primary hypertensive patients. Extensive studies are necessary to eluciate long-term effects of rhEPO in children.
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PMID:[Treatment of renal anemia with recombinant human erythropoietin]. 271 49

The amount of urinary calcium excretion is an useful marker for distinction between patient with preeclampsia and normal pregnancy of chronic hypertension has been reported. This study was performed to investigate the extent and the etiology of decrease in urinary calcium excretion in toxemia of pregnancy. The subjects in this study were 20 patients with severe toxemia of pregnancy (group T) and 20 subjects with normal pregnancy (group N). In these subjects, serum calcium (s-Ca), phosphate (s-Pi) and uric acid (s-UA) and urinary calcium (u-Ca), phosphate (u-Pi) and uric acid (u-UA) were measured. The values of u-Ca and u-Pi in the group T were significantly decreased than the group N (p less than 0.001, p less than 0.01). The values of s-Ca and s-Pi made no distinction between group T and group N. There was significant relationships between u-Ca and, s-UA (r = -0.70), clearance of UA (r-0.82), Ccr (r = 0.64), and FEca: Cca/Ccr (r = 0.87). These results indicated that the decrease of u-Ca was evident in severe toxemia of pregnancy. And the decrease of u-Ca has resulted from increase of tubular reabsorption. The change of u-Ca of patients with toxemia was studied. After the onset of toxemia, u-Ca was decreased rapidly (less than 50 mg/day) and u-Ca was restored to the normal range (more than 100 mg/day) promptly after delivery. The value of u-Ca was over 100 mg/day in the second pregnancy that developed on toxemia of pregnancy among the cases who has severe toxemia in the first pregnancy. However, toxemia of pregnancy have relapsed in the case with low u-Ca excretion of less than 100 mg/day during the second pregnancy.
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PMID:[Urinary calcium excretion in toxemia of pregnancy]. 274 5

A retrospective study of 89 patients with surgically proven primary hyperparathyroidism was done to gain insight into the pathogenesis of hypertension associated with this condition. The 43 patients (48%) who were hypertensive did not differ significantly from the normotensive patients with regard to age, sex, serum calcium and phosphate levels, and creatinine clearance. However, the mean serum magnesium level was significantly lower in hypertensive hyperparathyroid patients (1.52 +/- 0.24 mEq/L) than in normotensive hyperparathyroid patients (1.76 +/- 0.18 mEq/L; P less than .001), irrespective of use of diuretics in the former group. Although some studies implicate hypomagnesemia in the pathogenesis of essential hypertension, we are unaware of any previous human study reporting a link between hypomagnesemia and hypertension associated with primary hyperparathyroidism. This study suggests that a low level of serum magnesium may play a role in the pathogenesis of hypertension associated with primary hyperparathyroidism, a finding that needs further evaluation.
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PMID:Hypomagnesemia and hypertension in primary hyperparathyroidism. 277 81

We studied the effect of hydrochlorothiazide, 50 mg daily, on Na,K-adenosine triphosphatase (ATPase) activity in the red cells of 10 black men with hypertension. We also examined net sodium and potassium movement in sodium-loaded, potassium-depleted, red cells. Treatment with hydrochlorothiazide resulted in a significant increase in mean ouabain-sensitive ATPase activity (+/- SEM) from 118.4 +/- 14.6 to 158.1 +/- 15.3 nmol phosphate released per milligram of protein (P = 0.0004). Ouabain-resistant ATPase did not change. Net sodium extrusion rose significantly, from 1.62 +/- 0.27 to 2.32 +/- 0.33 mmol/L/hr (P = 0.0275). We postulate that the enhanced activity of the Na,K pump results from the volume contraction induced by the diuretic. This interpretation is consistent with the concept that the Na,K pump is inhibited in volume expansion and volume-expanded hypertension. The finding of enhanced pump activity in subjects given treatment with hydrochlorothiazide suggests a possible mechanism of the antihypertensive action of diuretic therapy.
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PMID:Effect of treatment with hydrochlorothiazide on the red cell Na,K-adenosine triphosphatase in men with hypertension. 282 24

We characterized the effect of a small, nonpeptidic molecule isolated from bovine hypothalamus on mammalian Na+, K+-adenosine triphosphatase (ATPase). This hypothalamic factor has been shown to inhibit ATPase activity of purified dog kidney enzyme reversibly with high affinity. This report reviews the mechanism of inhibition. Hypothalamic factor inhibits Na+, K+-ATPase only from the extracellular surface. It prevents the phosphorylation from magnesium and inorganic phosphate of the active site aspartate residue of Na+, K+-ATPase and stabilizes the enzyme in an E2 conformation, preventing a sodium-induced shift from E2 to E1. Binding and dissociation reactions of hypothalamic factor in cultured renal tubular epithelial cells show a time frame different from that in isolated membranes and consistent with physiological relevance. A possible mechanism for the physiological regulation of Na+, K+-ATPase, including a cycle of binding and rapid dissociation in intact renal tubular cells, is discussed.
Hypertension 1987 Nov
PMID:Regulation of Na+, K+-ATPase by the endogenous sodium transport inhibitor from hypothalamus. 282 68

We studied the effect of converting enzyme inhibition with enalapril on the natriuresis observed after administration of atrial natriuretic factor (human ANF-[99-126], given as a 100-micrograms bolus i.v. injection) in eight healthy humans consuming a 100 mmol sodium diet. Without enalapril, sodium excretion rose from 127 +/- 19 (mean +/- SE) to 437 +/- 103 mumol/min in the first 20 minutes after ANF was administered. Clearance studies performed during maximal water diuresis indicated a rise in glomerular filtration rate (inulin clearance), free water clearance, phosphate, lithium, uric acid, and magnesium excretion. Four days of enalapril (20 mg b.i.d.) increased effective renal plasma flow (p-aminohippurate clearance) and reduced blood pressure (from 114/71 +/- 2/2 to 105/60 +/- 2/1 mm Hg). Under these conditions baseline sodium excretion was not different from the control study, but it rose less after ANF (from 117 +/- 22 to 242 +/- 63 mumol/min), and the increments in glomerular filtration rate, free water clearance, phosphate, lithium, uric acid, and magnesium were all blunted and nonsignificant. In addition, effective renal plasma flow tended to fall; this effect was not observed when ANF was given without enalapril. These results support the notion that the effects of ANF on renal hemodynamics and on tubular sodium handling depend on renal angiotensin II and that blood pressure reduction may interfere with the ANF-induced natriuresis.
Hypertension 1988 Feb
PMID:Enalapril attenuates natriuresis of atrial natriuretic factor in humans. 283 Jan 88


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