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

The renin-angiotensin system appears to play a major role in the regulation of sodium excretion and fluid intake in a wide variety of animal species from mammals to teleosts. In mammals the system has evolved further importance in terms of blood pressure homeostasis. This hormonal system in all species appears to involve a serum protein prohormone, angiotensinogen, a proteolytic enzyme, renin, and angiotensin I, the decapeptide product of the reaction between renin and angiotensinogen. The importance of this system to the organism appears to correlate directly with the necessity to conserve sodium while an abnormality of this process may underlie the development of hypertension in man. As the starting point of the system, angiotensinogen assumes special importance as a possible index of evolutionary development. In addition, it has been known for many years that human (viz. primate) angiotensinogen differs from that found in other mammals in its inability to be a substrate for animal renins while animal angiotensinogens readily react with human renin. Thus, the enzymatic specificity appears to reside with the prohormone. The biochemical basis for this difference is unresolved due primarily to the lack of purified human angiotensinogen. In this paper we describe methods for the purification of human angiotensinogen which have direct applicability to animal angiotensinogens. Our approach utilizes ammonium sulfate precipitation, Sephadex G-150 chromatography, multiple isoelectric focusing, and concanavalin A-Sepharose affinity chromatography. With the availability of highly purified human angiotensinogen we compared the molecular weights, heterogeneity, isoelectric points, and thermal lability of hog, rabbit, and human angiotensinogen in order to define the biochemical basis of the species variation in renin reactivity...
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PMID:Human angiotensinogen. Purification partial characterization, and a comparison with animal prohormones. 1 60

The authors report a series of 22 cases of subdural hematomas in patients submitted to anticoagulant therapy. A review of the literature finds 150 cases. Subdural hematomas occurs in about one third of the patients presenting hemorrhage of central nervous system related to anticoagulant therapy. Among subdural hematomas of any cause, the possible role of a previous anticoagulant therapy is stressed in 4,8 to 14% of cases. In most cases, long term anticoagulants were indicated for arterial or heart (ischemic) lesions (16/22 cases). In 6 cases, anticoagulants were indicated for prevention or treatment of pulmonary embolies. In 18 cases, anticoagulant drug is from the group of dicoumarol or phenylindanedione. In 3 cases, the only anticoagulant given to patient was heparin. Pathogenic study suggests that hypocoagulability might not always be the only factor of bleeding: high blood pressure, other drugs and head trauma (10 cases) are often associated. Clinical features, in our series, are similar to those encountered in cases of subdural hematoma of any cause. According to the existence of a cranial injury and to the chronology of anticoagulant therapy, the authors divide their 22 patients into 3 groups. The use of protamin sulfate or human plasma fraction PPSB provides in few minutes a normal coagulability. Neurosurgical treatment in all our cases evacuated in 11 patients a chronic subdural hematoma, in 2 cases an acute, and in 9 cases a subacute hematoma. Results were fair in 19 patients with no sequelae. 3 patients died during the immediate post-operative period. The authors conclude by stressing several preventive measures.
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PMID:[Subdural hematoma and anticoagulant therapy]. 6 69

The metabolic clearance rate of dehydroisoandrosterone sulfate (MCRDS) was determined prospectively in gravidas with and without chronic essential hypertension. In normotensive patients, the MCRDS increased in linear fashion throughout pregnancy. In patients with chronic essential hypertension the MCRDS also increased progressively, but at higher values than in normotensive subjects. In normotensive gravidas who ultimately developed pregnancy-induced hypertension, the MCRDS increased progressively at a higher level than in gravidas who remained normotensive until approximately 4 weeks prior to the onset of clinical symptoms, at which time the MCRDS slowly decreased. Similarly, in gravidas with chronic hypertension who developed superimposed pregnancy-induced hypertension, the MCRDS increased progressively at higher levels than all groups studied until approximately 4 weeks prior to onset of hypertension, when a progressive decline in the MCRDS began.
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PMID:Metabolic clearance rate of dehydroisoandrosterone sulfate. V. Studies of essential hypertension complicating pregnancy. 12 16

The metabolic clearance rate of dehydroisoandrosterone sulfate (MCRDS) was measured in 11 women during an eclamptic episode, and the subjects were then followed for at least 5 years. The MCRDS was usually decreased in primigravid women with eclampsia. However, in eclamptic primigravid women who later developed essential hypertension and/or recurrent hypertension in subsequent pregnancies the MCRDS was elevated. Also, in multiparous women with chronic essential hypertension plus superimposed eclampsia, the MCRDS was increased to above normal values.
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PMID:Metabolic clearance rate of dehydroisoandrosterone sulfate. VI. Studies of eclampsia. 12 17

Alterations in steroidogenesis have been demonstrated in experimental and human hypertension. It is highly likely that increased secretion of the nonaldosterone mineralocorticoid deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) may initiate or perpetuate hypertension, or both. It is possible that 16 beta-hydroxydehydroeplandrosterone (16beta-OH-DHEA) directly induces the hypertensive process in animals. The significance of the findings of increased secretion of 16 alpha, 18-dihydroxy-11-deoxycorticosterone (16alpha, 18-diOH-DOC) and dehydroepiandrosterone sulfate (DHEA-S) cannot now be appreciated. Neither has been examined experimentally for its ability to induce hypertension, and the former compound is not a mineralocorticoid. It does possess the curious property of increasing mineralocorticoid activity of other steroids, by altering either their metabolism or mode of action. Variations in the mineralocorticoid hypertensive syndrome or, more aptly, the steroid hypertensive syndrome could account for the hypertension in a substantial portion of patients with reduced plasma renin activity.
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PMID:New mineralocorticoids and adrenocorticosteroids in hypertension. 13 92

Experimental segmental renal artery embolization was performed to evaluate the feasibility of therapeutic segmental renal embolization. In group 1, a two kidney dog model, segmental embolization of the right kidney was performed in ten dogs using Gelfoam, Silastic elastomer and barium sulfate. In group 2, a one kidney dog model, segmental embolization of left kidney was performed using Gelfoam and Silastic elastomer. In the remaining three dogs of group 2, embolization was not done for control. Sequential blood pressure measurements, plasma renin activities and renal arteriograms were obtained. Three dogs in group 2 died following unintentional complete renal embolization. Seventeen of the 18 dogs of the entire study remained normotensive after embolization. One dog had persistent hypertension develop which was controlled by a second, total renal embolization. The results suggest that therapeutic segmental renal embolization is a feasible method for treating segmental renal disease.
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PMID:Evaluation of a new method for treating segmental renal disease. 43 88

This point of view encountered in the treatment of pregnancy-induced hypertension enumerates the most common problems encountered when treating the disease. These problems include: terminology, etiology and pathogenesis, known facts, failure to identify the patient, loss of life for mother and baby, complications, recognition of early disease, and treatment not uniform or individualized. The severe forms of the disease are preventable and should never occur, but once present they should yield a zero maternal mortality rate and a fetal salvage of greater than 90%. Proper therapy of severe disease is primarily the use of pharmacologic doses of magnesium sulfate given intravenously and the prevention of a cerebral vascular accident in the mother. Induction of labor and removal of the products of conception will cure the disease.
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PMID:Problems encountered in the treatment of pregnancy-induced hypertension. A point of view. 68 45

Hypertension and hyperpotassemia that were accompanied by normal plasma aldosterone and low renin levels and were responsive to chlorothiazide administration were found in a 29-year-old patient and two decades later in his 21-year-old son. Their renal function is normal, including response to sodium sulfate, mannitol, and aldosterone infusions. Adrenal insufficiency was excluded. The renin-aldosterone system was proved intact by physiological and pharmacologic stress and angiotensin-II infusion. Also normal were values for blood counts, blood volumes, and erythrocyte and exchangeable body potassium. The postulation of a defective cell membrane impeding potassium influx is supported by the failure of glucose and insulin infusions to substantially reduce hyperpotassemia. In the context of a hereditary disorder (the pedigree, compatible with autosomal dominant inheritance, includes five affected in two generations), hypertension is a second phenotypic character of a single defective pleiotropic gene although its pathogenesis remains unclear.
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PMID:Familial hyperpotassemia and hypertension accompanied by normal plasma aldosterone levels: possible hereditary cell membrane defect. 71 48

In order to clarify the molecular basis of the unique features of rat renin (EC 3.4.99.19) and to provide materials and basic information for high blood pressure studies in rats, renin was purified from rat kidney. The final step of purification on CM-cellulose separated renin into three major isoenzyme peaks, R-I, R-II, R-III, and an additional minor peak. These preparations were judged homogeneous by multiple criteria, and the isoenzymes were found to have similar amino acid compositions. The amino acid composition is also closely analogous to hog renin, except that rat renin has a higher cysteine content. In contrast to hog renin, the rat enzymes do not contain amino sugars, yet are apparently glycoproteins as judged by their affinity for concanavalin A. The molecular weights of R-I, R-II, and R-III were estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis to be 37 000, 36 000 and 35 000, respectively. The isoelectric points were 5.05, 5.15 and 5.22, respectively. The specific activities of the purified enzymes (determined using rat plasma as substrate) were 615, 626 and 452 Goldblatt units/mg, respectively. Comparison of activities with the hog- and rat-derived substrates indicated a preference for that from the rat. The reaction of the rat enzymes with a synthetic peptide substrate had a similar catalytic rate constant to the hog enzyme, indicating close similarity in the active site region of the two enzymes.
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PMID:Rat renin: purification and characterization. 71 49

The hemodynamic effects of long term feeding of sympathomimetic amines (SPMA) to swine were studied. Three groups of female swine (N = 20 for each group) were fed either aminorex fumarate, d-amphetamine sulfate, or dextrose (control) for as long as 8 months in dosages up to 15 mg/kg/day. After 4 months of this feeding regiment, the weight gain of the pigs fed either aminorex or amphetamine was significantly less than the control animals. Hemodynamic measurements on awake swine indicated no elevation of pulmonary arterial blood pressure in the pigs fed SPMA. Measurement of systemic hemodynamics revealed that cardiac index was lower in the treated pigs than in control animals, but that heart rate and systemic arterial blood pressure were not altered by the drugs. In addition to baseline measurements of hemodynamic variables, the animals were exposed to acute hypoxia (12 percent O2 in N2) for 5 minutes. Although pulmonary arterial blood pressure increased similarly in the 3 groups of pigs, total pulmonary resistance increased to a greater extent in the pigs fed SPMA, indicating perhaps an enhancement of the hypoxic pulmonary pressor response after chronic ingestion of either amphetamine or aminorex. In a limited number of pigs, SPMA were fed for a period of 8 months, of which the last 3 months were during pregnancy. Hemodynamic measurements on sedated (metomidate, IV) swine revealed no difference in pulmonary arterial blood pressures between treated and control animals. We conclude that chronic ingestion of large doses of aminorex or amphetamine in swine does not lead to pulmonary arterial hypertension, but that slight reductions in cardiac output and subtle alterations in the pulmonary pressor response to acute hypoxia may occur.
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PMID:Hemodynamic effects of long term feeding of sympathomimetic amines to swine. 73 Nov 86


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