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

A young woman was referred for nephrologic evaluation of hypertension and a curious desire for table salt. Suspicion of iron-deficiency anemia arose only after it was determined that sodium balance was achievable during supervised sodium restriction. This salt craving abated within 2 weeks of initiation of iron replacement therapy. Although pica is a common manifestation of iron deficiency, this appears to be the first reported case of salt pica secondary to iron deficiency.
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PMID:Sodium chloride pica secondary to iron-deficiency anemia. 396 72

Acute hypertension was produced in rats by the infusion of angiotensin amide for 2 to 4 hours. These animals were injected intravenously prior to sacrifice with either colloidal carbon or iron dextran particles. The mesenteric vessels from hypertensive and control animals were processed for electron microscopy. Ultrastructural alterations are found in dilated segments of small arteries. Initially there is severe contraction of medial smooth muscle cells and the formation of processes of smooth muscle cytoplasm. This is followed by lysis of cell processes and bodies, and passage of plasma and colloidal iron into the media. Subsequently, carbon, platelets, fibrin and cellular debris are seen within these foci of medial necrosis. These changes appear as a sequence whose severity reflects the duration of the angiotensin infusion and degree of elevation of the systolic pressure. The morphologic alterations are discussed in relation to the generalized increase in vascular permeability that is associated with the hypertensive state.
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PMID:The cellular pathology of experimental hypertension. 7. Structure and permeability of the mesenteric vasculature in angiotensin-induced hypertension. 412 63

Sephadex particles (20-80 mu in size) were injected into the abdominal aorta of 134 male Sprague-Dawley rats near the renal arteries. In 31 rats, the right kidney was then removed. The Sephadex particles lodged in glomerular capillaries, afferent glomerular arterioles and interlobular arteries, creating renal infarcts, some of which were grossly visible. Shortly after injection, arterial blood pressure rose significantly in most animals. The hypertension in uninephrectomized rats was not demonstrably different from that in rats with two Kidneys. Severity and duration of hypertension (up to 8 months) were positively correlated with the number of Sephadex particles in renal vessels, and there was also a positive correlation between the degree of hypertension and serum urea nitrogen levels, and between degree of hypertension and degree of cardiac hypertrophy. The vascular permeability in acutely hypertensive rats was abnormal, as judged from penetration of iron-dextran into vessel walls. This experimental model resembles atheromatous microembolic renovascular disease, which may play a significant role in the pathogenesis of unexplained hypertension in patients with advanced aortic atherosclerosis.
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PMID:Microembolic renal disease in rats induced with sephadex. 425 58

A middle-aged man presented with weight loss, hypokalemic alkalosis, diabetes, hypertension, and generalized melanosis. Marked elevation of urinary free cortisol (655 micrograms/24 h) and plasma ACTH (2445 PG/ML) SUGGESTED THE DIAGNOSIS OF ECTOPIC ACTH syndrome. The plasma concentrations of cortisol and urinary 17-hydroxycorticosteroids increased paradoxically during the administration of dexamethasone without a corresponding change in the plasma ACTH level. Metyrapone administered over 24 h also markedly incrased both urinary free cortisol and 17-hydroxycorticosteroids. Selective venous sampling of plasma ACTH did not reveal a gradient between jugular vein and peripheral venous blood. The laboratory findings supported the diagnosis of ectopic ACTH syndrome. However, belated occurrence of visual changes necessitated surgical exploration, resulting in the diagnosis of pituitary carcinoma. A fluorescent antibody to ACTH reacted strongly with the atypical pituitary cells. This rare case documents that severe melanosis in Cushing's disease can occur without prior adrenalectomy and is consistent with the diagnosis of pituitary carcinoma. Furthermore, melanosis observed in patients with pituitary carcinoma is associated with ACTH levels similar to those occurrring in the ectopic ACTH or Nelson's syndrome.
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PMID:Pituitary carcinoma mimics the ectopic adrenocorticotropin syndrome. 624 43

A 93,000 molecular weight protein (HBP.93) which binds hemin and protoporphyrin IX with high affinity has been isolated from rabbit serum using affinity chromatography on hemin-conjugated agarose. The amino acid composition of this protein is unique in that the proline and histidine contents are remarkably high (16.6 and 9.9 mol %, respectively). A large increase in the absorbance of the Soret region arises from the heme-protein interaction. The spectrophotometric titration showed that the protein can bind 25-35 mol of hemin/mol of protein. The apparent dissociation constant was estimated to be 1-4 X 10(-7) M for hemin at pH 7.4 and approximately 10(-6) M for protoporphyrin IX at pH 9.2. The similarity of the difference spectrum of heme-HBP.93 complex to that of heme-hemopexin complex suggests that a bisimidazol-type coordination of heme iron is involved in the binding. The extremely high capacity of HBP.93 to bind heme is also demonstrated by a large increase in the sedimentation velocity of the protein upon heme binding. The native heme-protein complex migrates faster than the heme-free protein in a polyacrylamide gel at pH 8.8; the increased mobility appears to be due to the charge on the carboxyl groups of the bound heme. Although the use of a hemin-agarose column has failed to reveal a protein of similar size and heme affinity in the sera of a number of other species, including man, the heme-binding properties and high histidine level of the human alpha 2-histidine-rich glycoprotein raise the possibility that the two proteins are related.
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PMID:A protein with multiple heme-binding sites from rabbit serum. 627 54

Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.
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PMID:[Diagnosis and treatment of adrenocortical tumors]. 631

During the past 20 years there have been great developments in the scientific understanding of the role of nutrition in health and physical performance. Epidemiological and physiological studies have provided evidence that certain forms of dietary behaviour may be linked with an increased risk of developing disorders such as high blood pressure, coronary artery disease and some cancers. This has resulted in dietary recommendations that are intended to reduce the incidence of these disorders in the community. The science of nutrition in relation to sports performance has progressed from empirical studies investigating the effects of dietary manipulations, such as restriction and supplementation, to the direct investigation of the physiological basis of the specific nutritional demands of hard physical exercise. This review is based on the premise that it is "what comes out' rather than "what goes in', which provides the clues to ideal nutrition for athletic performance. Various aspects of the physical demands of athletic exercise are viewed as stresses that induce specific biochemical, and hence nutritional, strains in the athlete. Training is the predominant demand in the athletic lifestyle. This is characterised by acute bouts of high power output. During one hour of hard training an athlete may expend 30% of his or her total 24-hour energy output. These high power outputs have important implications for energy substrate and water requirements. Carbohydrate, specifically muscle glycogen, is an obligatory fuel for the high power outputs demanded by athletic sports. Muscle glycogen is a limiting factor in hard exercise because it is held in limited amounts, utilised rapidly by intense exercise, and fatigue occurs when it is depleted to low levels in the active muscles. Liver glycogen may also be exhausted by hard exercise and low blood glucose contributes to fatigue. High sweat rates are demanded during severe exercise and large water deficits commensurate with energy expenditure are incurred during extended periods of hard training and competition. Salt, potassium, and magnesium are lost in nutritionally significant amounts in the sweat, but vitamins and trace elements are not. Adaptive mechanisms protect athletes against electrolyte depletion. Iron loss in sweat may contribute to the iron deficiency seen in some endurance runners. Protein is degraded and amino acids are oxidised during physical exercise. Protein is also retained during muscle building training. Recent investigations indicate that the minimal protein requirements of athletes may be substantially higher than those for sedentary persons.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and sports performance. 639 Jun 9

The effects of acute angiotensin II (AII) induced hypertension on renal hemodynamics, urinary excretory rates, and clearances of endogenous proteins, together with colloidal iron staining and numerical density of differently charged ferritins in glomerular basement membrane (GBM) have been studied. AII decreases para-aminohippurate clearance (63%) more than glomerular filtration rate (GFR) (42%), resulting in an increased filtration fraction (54%). Simultaneously, large increments in the excretory rates and clearances of albumin and IgG2a occur. The number of native ferritin particles per unit volume of GBM and its different layers increases significantly in both superficial and juxtamedullary glomeruli as a result of acute hypertension. In contrast, the number of cationized ferritin particles per unit volume of GBM as well as colloidal iron staining of GBM and adjacent cell membranes remain unchanged, irrespective of AII treatment. The results demonstrate that acute AII-induced hypertension enhances glomerular permeability to proteins of different size and shape in the absence of detectable alterations in the fixed negative charges of the GBM. Since both RBF and GFR are decreased, the increased transglomerular passage of proteins in acute hypertension appears to be due to an increase in the pore size of the glomerular filter, induced possibly by either high intracapillary pressure and/or a direct action of AII on GBM constituents.
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PMID:Characterization of glomerular permeability and proteinuria in acute hypertension in the rat. 648 64

Acute hypertension induced by intravenous infusion of angiotensin II (AII) leads to enhanced transglomerular passage of albumin and IgG, as demonstrated by electronmicroscopic immunoperoxidase techniques. Although no morphological damage of the capillary wall was detected, significant amounts of macromolecules were present in the mesangial region. On a functional basis, a 42% decrease in glomerular filtration rate and a 63% decline in p-aminohippurate clearance were seen, resulting in a 54% increase in the filtration fraction. Quantitative measurements of albumin and IgG2a clearances showed a 90- and 15-fold increase, respectively. Similarly, the concentration of native ferritin particles in the glomerular basement membrane (GBM) increased 11-fold. On the other hand, the number of cationized ferritin particles and the staining properties of GBM to colloidal iron were not altered. These observations indicate that acute AII-induced hypertension affects glomerular permeability to proteins of different size and shape, possibly by increasing the pore size of the glomerular filter by either high intracapillary pressure and/or a direct action of AII on GBM constituents.
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PMID:Glomerular permeability in acute hypertension. 654 34

We examined sera from 159 patients with ischemic heart disease and hypertension and from 50 apparently healthy control subjects for content of trace elements, cholesterol, triglyceride, and enzymes. Concentrations of copper, cobalt, cholesterol, and triglyceride were increased in all patients, but calcium was decreased in patients with hypertension, acute myocardial ischemia, and acute myocardial infarction. Also accompanying acute myocardial infarction were decreased concentrations of zinc and iron but increases in nickel, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Magnesium concentration was lower in patients with acute myocardial ischemia. In acute myocardial infarction, the concentrations of copper, zinc, and iron were higher after 21-30 h (as compared with the values at 0-10 h), by which time concentrations of calcium, magnesium, cobalt, and alanine aminotransferase had decreased. The variation in concentration of trace elements in serum from cases of ischemic heart disease and hypertension corresponds to the severity of the disorder.
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PMID:Trace elements in serum from Pakistani patients with acute and chronic ischemic heart disease and hypertension. 671 25


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