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

The mechanisms and myocardial alterations associated with NO-deficient hypertension are still far from clear. The aim of the present study was to focus on the enzyme histochemical and subcellular changes in the heart of L-NAME treated rats, as well as to examine the influence of captopril treatment. Wistar rats were administered either L-NAME (40 mg/kg/day) alone or together with captopril (100 mg/kg/day) for a period of 4 weeks. A significant increase of blood pressure confirmed the reliability of the model. The results showed that long-lasting L-NAME administration was accompanied by a decrease of endothelial NO-synthase activity and by a significant local decrease of the following enzyme activities: capillary-related alkaline phosphatase, 5'-nucleotidase and ATPase (but not dipeptidyl peptidase IV) and cardiomyocyte-related glycogen phosphorylase, succinic dehydrogenase, beta-hydroxybutyrate dehydrogenase and ATPases. No activity of these enzymes was found in the scar, whereas a marked increase of alkaline phosphatase and dipeptidyl peptidase IV activities was found in the foci of fibrotization. Histochemical changes correlated with subcellular changes, which were characterized by 1) apparent fibroblast activation associated with interstitial/perivascular fibrosis, 2) heterogeneous population of the normal, hypertrophic and injured cardiomyocytes, 3) enhancement of the atrial granules and their translocation into the sarcolemma, and 4) impairment of capillaries as well as by induction of angiogenesis. Similar alterations were also found in the heart of captopril co-treated rats, despite of the significant suppression of blood pressure. The results indicate that NO-deficient hypertension is accompanied by metabolic disturbances and ultrastructural alterations of the heart and these changes are probably not induced by the renin-angiotension system only.
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PMID:Chronic disturbances in NO production results in histochemical and subcellular alterations of the rat heart. 1080 8

Monogenic or single-gene forms of human hypertension result from mutations involving regulatory elements of the renin-angiotensin-aldosterone system (RAAS) or occur in syndromes associated with hereditary pheochromocytoma. RAAS gain-of-function mutations result in sodium retention, suppression of plasma renin activity, and often, but not invariably, hypokalemia. Hereditary RAAS syndromes result from intrinsic renal abnormalities (apparent mineralocorticoid excess and Liddle's syndromes) or from mineralocorticoid excess states (congenital adrenal hyperplasia and glucocorticoid-remediable aldosteronism). In the hereditary pheochromocytoma syndromes many asymptomatic individuals are identified because they are at-risk individuals in kindreds with a pheochromocytoma-predisposing syndrome. On the other hand, up to 25% of subjects with presumed "sporadic" pheochromocytoma have germline mutations in one of four pheochromocytoma susceptibility genes (the RET proto-oncogene, von Hippel-Lindau gene, neurofibromatosis F1 gene, and succinate dehydrogenase subunit D and succinate dehydrogenase subunit B genes). Hereditary pheochromocytomas are typically intra-adrenal and bilateral and patients typically present at younger ages compared with sporadic pheochromocytoma.
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PMID:Screening for genetic causes of hypertension. 1241 72

Phaeochromocytomas are rare neuroendocrine tumours with a highly variable clinical presentation but most commonly presenting with episodes of headaches, sweating, palpitations, and hypertension. The serious and potentially lethal cardiovascular complications of these tumours are due to the potent effects of secreted catecholamines. Biochemical testing for phaeochromocytoma is indicated not only in symptomatic patients, but also in patients with adrenal incidentalomas or identified genetic predispositions (eg, multiple endocrine neoplasia type 2, von Hippel-Lindau syndrome, neurofibromatosis type 1, and mutations of the succinate dehydrogenase genes). Imaging techniques such as CT or MRI and functional ligands such as (123)I-MIBG are used to localise biochemically proven tumours. After the use of appropriate preoperative treatment to block the effects of secreted catecholamines, laparoscopic tumour removal is the preferred procedure. If removal of phaeochromocytoma is timely, prognosis is excellent. However, prognosis is poor in patients with metastases, which especially occur in patients with large, extra-adrenal tumours.
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PMID:Phaeochromocytoma. 1611 4

To assess the prevalence of genetic mutations in nonsyndromic pheochromocytoma/paraganglioma (PHEO/PGL) patients we have performed a systematic search for mutations in the succinate dehydrogenase (SDH) B, C, and D subunits, von Hippel-Lindau (VHL), and RET genes by direct bidirectional sequencing. Patients were selected from the medical records of hypertension centers. After exclusion of syndromic patients, 45 patients with familial (F+, n=3) and sporadic (F-, n=42) cases of isolated PHEO/PGL were considered. They included 35 patients with PHEO, 7 with PGL, and 3 with head/neck PGL (hnPGL). Three patients with PHEO (2F-, 1F+) presented VHL mutations (P86A, G93C, and R167W), six with PGL (4F-, 2F+) were positive for SDH or VHL mutations (SDHB R230G in two patients, SDHB S8F, R46Q, R90Q, and VHL P81L in one subject each), and one with hnPGL carried the SDHD 348-351delGACT mutation. We have also detected missense (SDHB S163P, SDHD H50R and G12S), synonymous (SDHB A6A, SDHD S68S), and intronic mutations that have been considered nonpathological polymorphic variants. No mutation was found in SDHC or RET genes. Our data indicate that germline mutations of VHL and SDH subunits are not infrequent in familial as well as in sporadic cases of nonsyndromic PHEO/PGL (overall, 12 of 45 probands, 22%). Accordingly, screening for such mutations seems to be justified. However, a more precise characterization of the functional relevance of any observed sequence variant and of other genetic and environmental determinants of neoplastic transformation is essential in order to plan appropriate protocols for family screening and follow-up.
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PMID:Genetic mutation screening in an italian cohort of nonsyndromic pheochromocytoma/paraganglioma patients. 1710 82

Pheochromocytoma (PHEO) is considered to be a rare cause of hypertension. However, if left untreated, PHEOs may lead to fatal hypertensive crises during anesthesia and other stresses. The diagnosis of PHEO is therefore extremely important. A 24-hour blood pressure (BP) pattern per se might be of some diagnostic value due to frequently observed higher BP variability as well as an attenuated night-time BP decrease. So far, germline mutations in five genes have been identified to be responsible for familial PHEOs: the von Hippel-Lindau gene, which causes von Hippel-Lindau syndrome, the RET gene leading to multiple endocrine neoplasia type 2, the neurofibromatosis type 1 gene, which is associated with von Recklinghausen's disease and the genes encoding the B and D subunits of mitochondrial succinate dehydrogenase (SDHB, SDHD), which are associated with familial paragangliomas and PHEOs. Genetic analysis should be offered to those patients with confirmed PHEO who are 50 years old or younger. Plasma-free metanephrines or urinary fractionated metanephrines seem to have higher diagnostic values compared to plasma or urinary catecholamines for the biochemical diagnosis of PHEO. Imaging with (123)I-metaiodobenzylguanidine or (18)F-fluorodopamine PET, if available, are in addition to CT/MRI useful for the detection of multifocal/extra-adrenal forms. Appropriate pharmacologic treatment with subsequent laparoscopic extirpation of PHEO is usually successful in benign forms. There is, however, no convincingly effective mode of treatment in malignant PHEOs.
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PMID:Recent advances in the diagnosis and treatment of pheochromocytoma. 1711 41

Pheochromocytomas are catecholamine-producing tumors presenting with various clinical symptoms, but mostly with headache, sweating, palpitations and hypertension. If not properly diagnosed, secretion of catecholamines may lead to fatal cardiovascular consequences. Biochemical testing for pheochromocytoma should be performed not only in symptomatic subjects or in subjects with adrenal incidentaloma but also in subjects with a genetic predisposition for pheochromocytoma (multiple endocrine neoplasia type 2, Von Hippel-Lindau (VHL) syndrome, neurofibromatosis type 1 (NF 1)and mutations of succinate dehydrogenase (SDH) genes). Once a pheochromocytoma is proven, computed tomography (CT), magnetic resonance imaging (MRI) and functional imaging with [(123)I]-MIBG may be used for tumor localization. Adequate medical pre-treatment is essential for successful operation which is performed in most cases by laparoscopy. After tumor removal, further follow-up is necessary due to possible recurrence. Although prognosis after tumor resection is excellent, a significant proportion of pheochromocytomas recur, some as metastases. Thus, appropriate follow-up is mandatory.
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PMID:Pheochromocytoma as a catecholamine producing tumor: implications for clinical practice. 1751 88

Pheochromocytomas (PHEOs) are rare neoplasms that produce catecholamines and usually arise from the adrenal medulla and are considered to be an adrenal paraganglioma (PGL). Closely related tumors of extraadrenal sympathetic and parasympathetic paraganglia are classified as extraadrenal PGLs. Most PHEOs are sporadic, but a significant percentage (approximately 25%) may be found in patients with germline mutations of genes predisposing to the development of von Hippel-Lindau disease, neurofibromatosis 1, multiple endocrine neoplasia type 1 (MEN1) and 2 (MEN2), and the PGL/PHEOs syndrome, based on the described mutations of the genes for succinate dehydrogenase subunit D (SDHD), B (SDHB), and C (SDHC). As one out of four PHEOs turns out to be a hereditary clinical entity, screening for genetic alterations is important, as it provides useful information for a rational diagnostic approach and management. This review discusses the genetics, the pathophysiology of hypertension, the clinical picture, the biochemical and imaging diagnosis, and the preferred therapeutic approach for PGLs/PHEOs. Furthermore, it emphasizes the need for genetic testing in cases with apparently sporadic PHEOs.
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PMID:Pheochromocytoma: an update on genetics and management. 1804 48

The integral area of gas discharge luminescence of the hand finger skin and the activity of succinate dehydrogenase in lymphocytes in blood smears from patients with food allergia and attendant hypertension has been measured. Succinate dehydrogenase in these patients was hyperactivated or inhibited as compared with healthy persons. At more substantial deviations of activity, a more clearly pronounced hypertension was observed. The area of luminescence of the skin in some patients was near the upper boundary of norm or was beyond its limits. A high degree of correlation (r = 0.85) between the two parameters has been revealed. At moderate and high succinate dehydrogenase activity, the parameters of gas-discharge visualization decreased; the inhibition of succinate dehydrogenase activity enhances, the gas-discharge visualization increases. This probably indicates the contribution to the irradiation from hand fingers of the superoxide formed in the respiratory chain of mitochondria in the region of coenzyme Q upon its incomplete reduction caused by the inhibition of succinate dehydrogenase.
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PMID:[A correlation of the intensity of the gas discharge luminescence of the skin and the activity of succinate dehydrogenase in blood lymphocytes in different states of the body]. 1848 11

Patients with a chronic brain ischemia of stages I-II on the background of hypertension and/or cerebral atherosclerosis are characterized by energy insufficiency of the metabolism, as estimated by the activity of succinate dehydrogenase in peripheral blood lymphocytes. Within the framework of randomized comparative investigation of the efficiency of actovegin and mexidol in the complex therapy of a chronic brain ischemia, positive dynamics in reduction of the clinical semiology, restoration of cognitive processes in the brain, and reduction of the expression of subjective manifestations of the disease is established. On this background, the administration of mexidol led to restoration of the energy exchange due to substrate effects of the Krebs cycle intermediates present in its structure.
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PMID:[Metabolic effects of mexidol in complex treatment of chronic brain ischemia]. 1914 May 8

These investigations are part of an attempt to study and interpret the intermediary metabolism of the kidneys in experimental renal hypertension. Hypertension was produced in dogs by the clamping procedure of Goldblatt and associates or by the silk perinephritis method of Page. Enzymatic studies were made by means of Warburg's manometric method. Cytochrome c was in addition determined spectrophotometrically. Tissue slices, homogenized tissue, and tissue extracts were used. A study of the cytochrome c concentration and the activities of the cytochrome oxidase and succinic dehydrogenase systems of kidneys from normal dogs and dogs with experimental renal hypertension was made. It was found that the cytochrome c concentration and the activities of the cytochrome oxidase and succinic dehydrogenase systems were markedly lower in the kidney slices and in the tissue suspensions from hypertensive dogs. Tissue suspensions and extracts of kidneys from hypertensive dogs showed an inhibitory effect on the activity of the cytochrome oxidase and succinic dehydrogenase, and the amine oxidase systems. Renin preparations also showed a marked inhibitory effect on the activities of cytochrome oxidase, succinic dehydrogenase, l-amino acid oxidase, and amine oxidase systems. A significant increase was found in the kidney of dogs whose other kidney had been removed or subjected to Goldblatt's or Page's technique in the activities of the cytochrome-cytochrome oxidase system, the succinic dehydrogenase system, and in the concentration of nucleotide-bound phosphorus, of flavin-adenine dinucleotide, and of the nicotinamide-adenine dinucleotides (coenzymes I and II). From the results of these studies it can be concluded that an increase in the concentration and activity of the respiratory enzymes precedes hypertrophy of the kidney. This can be explained by the assumption that an increase in the activity of the respiratory biocatalysts acts as a stimulus for cell growth and multiplication.
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PMID:THE METABOLISM OF THE KIDNEY IN EXPERIMENTAL RENAL HYPERTENSION : II. THE CONCENTRATION OF CYTOCHROME C AND THE ACTIVITIES OF THE CYTOCHROME OXIDASE AND OF THE SUCCINIC DEHYDROGENASE SYSTEMS IN THE KIDNEY OF DOGS WITH EXPERIMENTAL RENAL HYPERTENSION. THE INHIBITORY EFFECT OF RENIN AND OF KIDNEY TISSUE PREPARATIONS FROM HYPERTENSIVE DOGS ON THE RESPIRATORY ENZYMES. 1987 97


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