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

Parallel morphometric, karyometric and ultrastructural studies of the aortic wall in Okamoto-Aoki rats with short term (3-6 months) and long-term (12-16 months) spontaneous hypertension have revealed a progressive thickening of the medial layer, which is associated with an increaase in the mean nuclear area of the arterial medial smooth muscles and reduction in their mean number per unit area. Electron microscopic studies have shown a multiplication of the intracellular components of aortic smooth muscle cells as a base for their enlargement, as well as small single foci of smooth muscle hyperplasia in the area of the innermost interlamellar space in parts of the aortic wall with intimal thickening. Results of these studies allow the conclusion, that hypertrophy is a reaction of arterial smooth muscle cells to an increased mechanical load in hypertension which, in turn, is responsible for the thickening of arterial with Hyperplasia - increase in smooth muscle cells' number in the media - played a subordinate role. The reaction of the aortic wall to elevate blood pressure is interpreted as a manifestation of the normally limited division capacity of smooth muscle cells in mammals, which does not allow an increase in its cellular components. The function of existing arterial smooth muscle smooth cells is enhanced, instead, by hyperplasia of their specific organelles and augmentation of their volume.
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PMID:Aortic smooth muscle cells reaction in rat spontaneous hypertension. 13 46

In the present study, arteriosclerotic change of the aorta was induced in rats. The effects of manidipine hydrochloride on the resulting hypertension and arteriosclerotic change were studied. In endothelium-injured cholesterol-fed Goldblatt 2K1C rats, moderate elevation of blood pressure was noted at 3, 4, and 5 weeks. Laboratory studies performed at the end of 6 weeks also showed hypercholesterolemia, accompanied by a reduction of triglycerides and HDL cholesterol. Regular doses of manidipine (200 or 500 mg/kg) resulted in a dose dependent inhibition of the blood pressure elevation and a reduction of HDL cholesterol, but had no effect on cholesterol or triglyceride levels. Morphological studies in endothelium-injured rats afflicted with hypercholesterolemia and hypertension, showed medial thickening and intimal hyperplasia. Hyperplasia of the intima was a result of excessive proliferation of the smooth muscle cells. These cells showed an unusually large number of fat droplets and were considered indicative of atheromatous plaque formation. In rats treated with manidipine, hyperplasia of the media was completely suppressed while hyperplasia of the intima was reduced by a minimum of 50%. This study demonstrated that hypercholesterolemia and hypertension produced arteriosclerotic change in endothelium-injured rats, which was inhibited by manidipine. It is not known whether antiarteriosclerotic action was involved in the antihypertensive effect of manidipine.
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PMID:Manidipine inhibits the progression of hypertension and atherosclerosis in endothelium-injured and cholesterol-fed Goldblatt 2K1C rats. 134 87

Idiopathic hyperaldosteronism was diagnosed in an 8-year-old castrated male Yorkshire Terrier, based on increased concentration of plasma aldosterone, hypertension, hypernatremia, decreased natriuresis, hypokalemia, and hyperkaluria. Unilateral adrenalectomy was performed after visualization of a nodule on the right adrenal gland. Hyperplasia of the zona glomerulosa and increased postoperative aldosterone concentrations supported the diagnosis of idiopathic hyperaldosteronism.
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PMID:Idiopathic hyperaldosteronism in a dog. 299 95

Renal tissue was obtained from 36 patients with renal cell carcinoma, some of whom received renal arterial embolization. The removed specimens was examined histopathologically and the concentration of some vasoactive substances in these patients was measured. Nephrectomy alone produced no discernible changes in blood pressure, vasoactive substances determined or histopathological findings of the kidney. Renal arterial embolization raised the blood pressure in association with the elevation of plasma renin activity (PRA) and urinary prostaglandin (PG) E2 excretion. A linear relationship was found to exist between PRA and mean blood pressure (r = 0.70, p less than 0.001). Hyperplasia of the juxtaglomerular (JG) apparatus, and high granularity of sudan black B granules in renomedullary interstitial cells were confirmed in removed kidneys of patients who had received embolization alone. Subsequently high renin production would be anticipated to influence overproduction of renal PG E2 in acute ischemic kidney in patients with renal cell carcinoma, and hypertension following renal arterial embolization appears to be caused by the hyperplasia of the JG apparatus.
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PMID:Hyperplasia of juxtaglomerular cells and renomedullary interstitial cells after renal arterial embolization in patients with renal cell carcinoma. 306 3

Hyperplastic carotid bodies from an 80-year-old woman with sustained systemic hypertension were examined ultrastructurally and compared with those from six normal subjects. Hyperplasia involved both elongated sustentacular and Schwann's cells, both of which were more numerous than normal. They formed concentric whorls around a diminished core of chief cells. The Schwann's cells adopted a peripheral position in each cell cluster, whereas the sustentacular cells were located closer to the central core. The characteristics of both types of cell were similar so that they could not be distinguished from each other in every instance. They were associated with numerous nerve axons with which they usually displayed a simple mesaxonal relationship. The myelin sheaths formed by Schwann's cells were well developed but those encountered in sustentacular cells were usually rudimentary. A few fibroblasts were also present, but generally the process of hyperplasia was not one of fibrosis; neither did it involve pericytes.
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PMID:Electron microscopy of carotid body hyperplasia. 654 24

The most pronounced hyperplasia of the juxtaglomerular apparatus (JGA) with the appearance of numerous rhombus-like protogranules in the epithelioid cell cytoplasm is found electronmicroscopically in the mesangioproliferative glomerulonephritis (GM) with hypertension while in the membranous FN the hyperplasia was the least pronounced. Hyperplasia of JGA in the fibroplastic GN was observed in the preserved glomeruli only. Morphometric evaluation in mesangioproliferative GN has shown that there is an inverse relationship between the volume of the interstitium and the renin activity in the blood plasma, the positive correlation between the volume of the interstitium and blood pressure and the negative correlation between the elliptical shape of the granules in the JGA epithelioid cells and the surface of the interstitium. Atrophic changes in the interstitial cells are found.
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PMID:[Juxtaglomerular apparatus and interstitial cells of the kidney medulla in glomerulonephritis]. 671 13

Essential hypertension is fundamentally a genetic disease which emerges because of environmental impact. The genetic factors involve intracellular abnormalities which affect calcium metabolism within smooth muscle cells and possibly within the heart and sympathetic nervous system. These abnormalities are influenced by one or more proteins of which calmodulin is a candidate. Sodium pump abnormalities may be primary but may be secondary feedback effects. Homeostasis keeps the blood pressure and cardiac function normal, but eventually becomes less effective. Such homeostasis is produced by negative feedback, but positive external factors also influence the eventual results. Gross homeostasis is provided by the baroreceptors, the renin-angiotensin-aldosterone system, etc. The malfunction of any one or any combination of these systems may produce or accelerate hypertension. Hyperplasia and hypertrophy of arteriolar smooth muscle play their role but also multiply the genetic cellular defects. It is possible that in the early history of man essential hypertension had an advantage which now has become obsolete because normotensive man's potential lifespan has been increased by modern civilization.
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PMID:The relation of genetics to essential hypertension: a review. 713 17

Hyperplasia of myocytes in cardiac adaptation is a rare event in the mammalian cardiac muscle. Recent findings support the concept that proliferation of myocytes in the adult mammalian heart may be induced after a prolonged increase in pressure load on the myocardium. To determine whether short-term hypertension leads to hyperplasia of myocyte nuclei in the rat heart renal hypertension was produced in 12 Wistar rats. As soon as hypertension occurred, bromodeoxyuridine (BrdU) (50 mg/kg/day) was injected intraperitoneally on three subsequent days. Twelve sham-operated rats served as controls. After 3 days, the left cardiac ventricle was excised and double-staining with anti-BrdU antibody and propidium iodide was performed to determine the phase of cell-cycle of the BrdU-positive cells by flow-cytometry. Immunohistochemical double-staining with desmin, smooth muscle actin, vimentin, and BrdU was done to classify the BrdU-positive cells. Most of the BrdU-positive cells were in the G0/G1-phase of the cell-cycle, suggesting cell proliferation or DNA-repair have taken place; polyploidy was not observed. In the hypertensive group (4.62% +/- 2.36) significantly more cells incorporated BrdU than in the control group (1.46% +/- 0.96). Immunohistochemically, the majority of the BrdU-positive cells consisted of fibrocytes, smooth muscle cells, and endothelial cells. Only 0.35% +/- 0.26 of cardiac myocytes in the normotensive group showed positive BrdU-staining compared to 0.48% +/- 0.32 in the hypertensive group. This difference was statistically not significant. This study showed that early after onset of hypertension proliferation of non-myocytes, but not of myocytes occurred. DNA synthesis is limited almost completely to the interstitial cells and does not occur in any significant extent in cardiac myocytes. In conclusion, hyperplasia of cardiac myocytes is not observed at early stages of hypertension, but it may develop at a late stage of cardiac adaptation.
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PMID:Early proliferative changes in hearts of hypertensive Goldblatt rats: an immunohistochemical and flow-cytometrical study. 887 76

Primary hyperaldosteronism (adrenal adenoma and idiopathic hyperplasia) is a disorder with hypertension, hypokalemia, elevated serum aldosterone and suppressed plasma renin activity. Hyperplasia is managed medically whereas adenomas are treated surgically. Selective adrenal venous catheterization and aldosterone measurement is a useful tool in making the distinction in 95% of cases. We report a case of bilateral idiopathic hyperplasia of the adrenal glands adequately treated with medications for 6 years followed by worsening. Selective catheterization was consistent with a right sided adenoma. Surgical removal of the right adrenal gland alleviated her symptoms. Pathological examination showed focal nodular hyperplasia. We propose that in the course of the disease the focal hyperplastic nodule became autonomous and behaved like an adenoma. Monitoring of patients with adrenal hyperplasia for recurrence of symptoms is prudent as surgery is beneficial in patients who develop an autonomous nodule.
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PMID:Idiopathic hyperplasia of the adrenal gland behaving like an aldosterone producing adenoma. 907 69

The high prevalence of Benign Prostate Hyperplasia and the increased demand for care of this condition, should compel us to plan for shared care models in parallel to Primary Care, in the way it has happened with entities such as HBP and Diabetes. The set of measurements to be adopted when sharing services with primary care is known as "shared care". This paper presents the first national experience of "shared care" with primary care in BPH. The project has consisted in a series of steps to increase awareness, train and make available for family physicians, a clinical practice guide defining the criteria for initial evaluation, medical treatment and referral of patients to Urology surgeries, including with the referral document the appropriate diagnostic tests. A Quality Commission has been created to study the level of compliance of the documentation used for referral to the specialist and the clinical histories of patients treated in primary care. The results obtained are significant and most studies carried out fulfill the requirements in 60% cases, which has allowed to reduce overcrowding in the Urology outpatient offices (4200 surgery visits saved/year in our environment), has provided easy access of patients to adequate diagnosis and treatment, as well as significant financial savings (30 million pesetas/year). In short "shared care" is a reality in our environment that allows a more effective, fast medical assistance and improved access to specialist care by reducing the demand of specialized surgery hours.
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PMID:[Shared care in BPH. First national experience]. 973 23


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