Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

A protein from rat kidney was characterized that had several properties common to a multigene family of fatty acid binding proteins identified in other tissues. The putative kidney fatty acid binding protein (FABP) was purified from the soluble fraction of kidney homogenates using gel filtration and ion exchange chromatography. It was relatively abundant, had an apparent molecular mass of 15.5 kDa as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, bound equimolar amounts of oleic acid, and could be distinguished from other FABPs on the basis of size, amino acid composition, and tissue distribution. Polyclonal antibodies to kidney FABP were obtained and used to show that only kidney contained the 15.5-kDa protein, although the antibodies also recognized a slightly larger and less abundant protein in kidney that also was present in bladder. Rat kidney also contained heart FABP, and the properties of both FABPs in rat kidney were compared. The distribution of both proteins within the kidney differed, with kidney FABP being localized almost exclusively within the cortex, whereas heart FABP was found both in cortex and medulla. Kidney FABP was expressed developmentally after the neonatal period, whereas heart FABP was present in both neonatal and adult kidney at comparable amounts. Hypertension induced by mineralocorticoids or infusion of angiotensin II caused a marked suppression of kidney FABP expression, whereas amounts of heart FABP in kidney were unchanged. The studies showed that rat kidney contains at least two FABPs, and that these proteins are differentially regulated, suggesting that functional differences between the proteins may exist.
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PMID:Properties and differential regulation of two fatty acid binding proteins in the rat kidney. 317 Jun 9

To investigate effects of systemic nicotine on mucus secretion from tracheal submucosal glands we anesthetized 13 ferrets (5 male, 8 female; average weight 1138 +/- 469 g, mean +/- SD) with pentobarbital (initial dose, 62 +/- 26, total dose, 90 +/- 26 mg/kg), cannulated the jugular vein for i.v. application of infusions and drugs and cannulated the femoral artery for determination of blood pressure, heart rate, blood cells, and blood gases. We opened the thorax, cannulated the trachea 1 cm above the carina and ventilated the lungs through the lower airways with a Harvard respirator. We placed an electromagnetic flow probe around the ascending aorta for measurement of cardiac output. We measured transpulmonary pressure as tracheal pressure with a strain gauge transducer. We created an isolated segment of trachea between the larynx and the tracheal cannula. We perfused the segment with medium M-199 containing 30 microCi/ml Na(2)35SO4 (35S) and we injected 100 microCi 35S intravenously. After 90 min we drained the radioactive solution from the luminal side and replaced it with nonradioactive medium which we collected at 5-min intervals for determination of nondialyzable radioactivity. At 25 min we injected nicotine sulfate (5 x 10(-7)-10(-5) M/kg) and continued to collect the perfusate every 5 min. Systemic nicotine had profound effects on circulatory and ventilatory variables and on gland secretion. Initial hypertension was followed by bradycardia and a fall in blood pressure and cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of systemic nicotine on mucus secretion from tracheal submucosal glands and on cardiovascular, pulmonary, and hematologic variables. 318 74

When intravenous magnesium sulfate is infused in women with pregnancy-induced hypertension, the hypermagnesemia does not result in lower Apgar scores. The mean maternal serum and cord magnesium levels at delivery were 5.3 +/- 0.72 and 5.3 +/- 1.1 mEq/dl, respectively. The most common negative Apgar score was assigned for color, not for muscle tone.
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PMID:The effects of magnesium sulfate therapy on Apgar scores. 318 36

In order to elucidate the mechanism of pregnancy-induced hypertension (PIH) from the point of view of vascular resistance, we measured the intracellular Na+ concentrations and the membrane Na+ effluxes using red blood cells from normal pregnant females and patients with PIH. We also discussed the influences of hormones such as estrogen, progesterone, dehydroepiandrosterone sulfate (DHAS), hydrocortisol, human placental lactogen (hPL), human chorionic gonadotropin (hCG), and prolactin and parathyroid hormone (PTH) on the membrane Na+ effluxes. The intracellular Na+ concentrations were lower and the Na+-K+-ATPase activities were slightly higher both in the luteal phase and in the first trimester of normal pregnancy than those in the follicular phase, after which the former gradually increased and the latter gradually decreased until term to the mean values of those in the whole menstrual period. In mild PIH, the intracellular Na+ concentrations were not significantly increased, and the Na+-K+-ATPase activities were significantly increased compared to those in the third trimester of normal pregnancy, which suggests the compensatory increase of the Na+-K+-ATPase activities as opposed to the increase of the intracellular Na+ concentrations. In severe PIH, the intracellular Na+ concentrations were significantly increased compared with those in the third trimester of normal pregnancy and slightly increased compared with those in mild PIH, whereas the Na+-K+-ATPase activities were slightly decreased compared with those in mild PIH, which indicates a breakdown of the compensatory increase of the Na+-K+-ATPase activities. The intracellular Na+ concentrations in PIH are significantly correlated to diastolic pressure, systolic pressure and mean blood pressure. When the male red blood cells were incubated with the hormone, dose-dependently the Na+-K+-ATPase activities were significantly elevated by hydrocortisol and slightly elevated by progesterone and hPL, and they were significantly depressed by estrogen and prolactin and slightly depressed by PTH. These results suggest that the peripheral vascular resistance might be increased in the third trimester of normal pregnancy compared with that in the first trimester because the intracellular Na+ concentrations were elevated, and the Na+-K+-ATPase activities in the cell membrane were decreased along the course of pregnancy as a result of the effects of various hormones in the maternal blood.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A study on the membrane Na+ efflux of pregnancy-induced hypertension (PIH)]. 320 19

The patient was admitted to our hospital at 19 and again at 22-yr of age for hirsutism and hypertension. Her baseline and ACTH-stimulated plasma 17-hydroxy pregnenolone, dehydroepiandrosterone and dehydroepiandrosterone sulfate were increased whereas plasma 17-hydroxy progesterone and androstenedione were normal and responded poorly to ACTH. Plasma deoxycorticosterone, corticosterone and cortisol baseline levels were normal, and they responded normally to ACTH. The plasma aldosterone concentration (PAC) was always high and responded well to ACTH, angiotensin III and furosemide-upright stimulation. However, plasma renin activity (PRA) was normal or slightly high, and responded normally to furosemide-upright stimulation and fluorohydrocortisone suppression. Dexamethasone (2 mg/day) for 1-2 weeks suppressed the androgens, cortisol and corticosterone levels. PRA and PAC were suppressed temporally, but PRA returned to normal and PAC to be a high level after 2 weeks of dexamethasone administration. Blood pressure was also reduced temporally but returned to a high level after 2 weeks of dexamethasone. These results indicate that primary aldosteronism and dexamethasone-suppressible hyperaldosteronism were not likely to be present, and unknown aldosterone stimulating factors which potentiated the action of endogenous angiotensin II or ACTH might be responsible for the hyperaldosteronism in this patient. We conclude that this patient had a mild and non-salt losing 3 beta-HSD deficiency in the zona reticularis with normal fasciculata and high glomerulosa function.
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PMID:Mild adrenal 3 beta-hydroxysteroid dehydrogenase deficiency with hyperaldosteronism. 322 46

Pre-eclampsia/eclampsia, or pregnancy-induced hypertension, is an uncommon but life-threatening complication of pregnancy associated with significant perinatal morbidity. When superimposed on underlying chronic hypertension, its impact on the fetus becomes even greater. Although the pathophysiology of the disease has not been fully defined, vasospasm appears to be the principal, underlying, etiologic mechanism. Therapy of the disease is principally aimed at controlling convulsions with magnesium sulfate and controlling hypertension with the antihypertensive agent hydralazine. Because development of the disease depends on the presence of trophoblastic tissue, the only true cure for pre-eclampsia/eclampsia is removal of the trophoblast through delivery of the infant. The timing and type of delivery is dependent on the severity of the disease and gestational age of the infant.
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PMID:Hypertensive disorders of pregnancy. 330 27

Hypertension is common in the elderly and is associated with higher morbidity and mortality, which may be decreased by effective blood pressure control. Many antihypertensive drugs, however, are not well tolerated by the aged. We treated 21 patients (ten men and 11 women) between ages 65 and 84 years (mean, 73.6 years) with guanadrel sulfate. All patients had received prior antihypertensive therapy, which either was ineffective or caused undesirable side effects. Average follow-up time was 17 months. Mean systolic pressure on enrollment was 188 +/- 17 mm Hg and mean diastolic pressure was 100 +/- 10 mm Hg. After treatment, the mean systolic pressure was 139 +/- 15 mm Hg and mean diastolic pressure was 82 +/- 8 mm Hg. Dosage varied from 5 to 30 mg/d with a mean of 16 mg/d. The only significant side effects were fatigue, dizziness, and dyspnea reported in four patients. Eleven patients took the medication as monotherapy and ten received diuretics or diuretics and beta-blockers as additional therapy. Our conclusion is that guanadrel is an effective, well-tolerated medication for treatment of hypertension in the elderly.
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PMID:Efficacy and safety of guanadrel in elderly hypertensive patients. 338 97

The adverse effects of protamine sulfate, used to neutralize the anticoagulant action of heparin, include systemic hypotension, pulmonary artery hypertension, thrombocytopenia and leukopenia. For further evaluation of protamine's mechanism of action, a three-part investigation was performed. In part I platelet-rich plasma (PRP) was prepared from canine blood samples (n = 6) taken before and 2 minutes after injection of protamine. In part II human PRP (n = 5) was preincubated with protamine or distilled water. Adenosine diphosphate-induced aggregation of protamine-treated platelets was unchanged, but thrombin-induced aggregation was inhibited in both canine and human preparations (p less than 0.05). In part III thrombocytopenia was produced in splenectomized dogs (n = 5), using microporous filters, to 4.5-8.4% of the initial platelet count. Protamine reversal of the heparinization caused hypotension (maximally -29 mmHg 90 s after protamine), but not pulmonary arterial hypertension. Leukopenia developed before additional thrombocytopenia appeared. Protamine-platelet interaction inhibits thrombin-induced platelet aggregation. Platelets may play an important role in the pulmonary pressure rise during protamine reversal, but do not mediate the systemic hypotension.
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PMID:The effect of protamine sulfate on platelet function. 338 50

Adrenal weights and histologic features in an autopsy population of 759 fetuses and neonates were correlated with the presence or absence of pregnancy-induced hypertension. Hypoplastic fetal adrenals with normal proportions of fetal and adult cortical layers (miniature histologic type) had combined adrenal weights less than 1 g, and were noted in 11 fetuses and neonates born to 39 mothers with pregnancy-induced hypertension, two born to 35 mothers with suggested pregnancy-induced hypertension, and 45 born to 685 mothers with no pregnancy-induced hypertension. Hypoplastic fetal adrenals were associated significantly with pregnancy-induced hypertension by chi 2 analysis (P less than .01). When a more stringent criterion for fetal adrenal hypoplasia was used (combined adrenal weight/body weight ratio of less than 1:1000), five cases were associated with pregnancy-induced hypertension, three with suggested pregnancy-induced hypertension, and seven with normal maternal blood pressures (P less than .001). This study confirms the relationship between pregnancy-induced hypertension and reduced fetal adrenal mass. We speculate that reduced production of dehydroepiandrosterone sulfate by the small adrenals may be related to maternal hypertension.
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PMID:Pregnancy-induced hypertension and congenital adrenal hypoplasia. 339 61

We designed the present study to clarify whether the development of nephropathy was accelerated by a combination of hypertension and non-insulin-dependent diabetes. Spontaneously hypertensive rats with non-insulin-dependent diabetes induced by neonatal streptozotocin treatment (25.0-75.0 mg/kg) were separated into severely or mildly diabetic groups according to their non-fasting plasma glucose levels at 12 weeks of age and the findings were compared with the data on a control group treated with citrate buffer alone. The natural courses of urinary excretion rate of total protein, the molecular composition by sodium dodecyl sulfate polyacrylamide gel electrophoresis with laser densitometer and N-acetyl-beta-D-glucosaminidase were measured in the three groups from 12 weeks until 36 weeks of age. Total urinary protein in the control group decreased with age (p less than 0.05), while in the mildly diabetic group changes were nil; in the severely diabetic group, however, the excretion rates of total urinary protein and high molecular weight protein consistently and progressively increased with age (p less than 0.05). The low molecular weight protein continuously decreased with age in the mildly diabetic and control groups (p less than 0.05), while in the severely diabetic group there was no decrease after 28 weeks of age. The urinary N-acetyl-beta-D-glucosaminidase markedly increased (p less than 0.05) in the severely diabetic group throughout the period compared with findings in the control group, but drastically decreased (p less than 0.05) in the mildly diabetic group with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early development of nephropathy in a new model of spontaneously hypertensive rat with non-insulin-dependent diabetes mellitus. 339 85


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