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

Hypertrophic adaptation of the left ventricle and blood vessels is a prominent feature of established essential hypertension. Presence of left ventricular hypertrophy in hypertension increases, independently of other risk factors, the risk for a number of the most important cardiovascular hypertensive complications. Available evidence indicates that left ventricular hypertrophy develops in close parallel with the peripheral vascular changes. Structural involvement can be detected already in early phases of borderline hypertension. The pathophysiology of structural changes in hypertension appears to be dependent on a complex interplay between genetic, hemodynamic, and humoral-metabolic factors.
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PMID:Pathophysiology of cardiovascular structural changes in hypertension. 153 85

Diabetic patients who develop proteinuria show a marked increase in cardiovascular morbidity and mortality. The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain, in part, obscure. However, there is now evidence that renal disease clusters in families and that genetic factors may be of central importance in determining susceptibility. Predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. Interestingly, fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first clinical signs of renal involvement are the appearance of microalbuminuria and a small elevation in arterial pressure. Mesangial expansion accompanies these changes. Microalbuminuria is associated with abnormalities of lipoprotein profiles and higher Na+/Li+ countertransport rates. The environmental changes brought about by diabetes could lead in susceptible individuals to increased systemic and intraglomerular pressures on the one hand and to mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities may further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered, involving reduction in renal function, further hypertension, proteinuria, glomerular obsolence and hyperlipidaemia, and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Risk factors for renal and cardiovascular disease in diabetic patients. 165 64

Among dialysis patients, only 23% have a normal echocardiogram, about 10% have recurrent or chronic congestive heart failure, and 17% have asymptomatic ischemic heart disease. The predisposing factors for congestive heart failure are dilated cardiomyopathy, hypertrophic hyperkinetic disease, and ischemic heart disease. Dilated cardiomyopathy, a disorder of systolic function, includes among its risk factors age, hyperparathyroidism, and smoking. Hypertrophic disease results in diastolic dysfunction, and its predictors include age, hypertension, aluminum accumulation, anemia, and, perhaps, hyperparathyroidism. Ischemic heart disease is due to the presence of coronary artery disease and also to nonatherosclerotic disease caused by the reduction in coronary vasodilator reserve and altered myocardial oxygen delivery and use. The clinical outcome of congestive heart failure is comparable to that of nonrenal patients with medically refractory heart failure. Left ventricular hypertrophy is an important independent determinant of survival. A subset have hyperkinetic disease with severe hypertrophy and have a bad survival, as low as 43% have a 2-yr survival after the first admission to hospital with cardiac failure. The prognosis for those with dilated cardiomyopathy is less severe but is worse than those with normal echocardiogram. The survival of patients with symptomatic ischemic heart disease was little different from that of patients without symptoms, suggesting that the underlying cardiomyopathies had an adverse impact on survival independent of ischemic disease. Much research needs to be undertaken on the risk factors, natural history, and therapy of the various types of cardiac disease prevalent in dialysis patients.
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PMID:The natural history of myocardial disease in dialysis patients. 183 84

Left ventricular hypertrophy in response to pressure overload may be modified by neurohumoral activation. To investigate the contribution of the renin-angiotensin system, we studied rats after banding of the ascending aorta that developed severe left ventricular hypertrophy associated with normal plasma renin but elevated cardiac angiotensin-converting enzyme (ACE) levels. Rats were treated with vehicle, ACE inhibitor (ramipril), angiotensin II type 1 receptor antagonist (losartan), or vasodilator (hydralazine) during weeks 7 through 12 after aortic banding. A significant regression of left ventricular mass index as determined by serial echocardiography was observed in ramipril- and losartan-treated groups during weeks 9 through 12 after banding, whereas hypertrophy further increased in vehicle- and hydralazine-treated groups. Twelve weeks after banding, relative left ventricular weights and myocyte widths were markedly increased in vehicle- and hydralazine-treated groups, whereas ramipril and losartan significantly reduced these parameters. In addition, molecular adaptations in left ventricular hypertrophy, such as upregulation of left ventricular atrial natriuretic peptide and downregulation of sarcoplasmic reticulum Ca(2+)-ATPase mRNA levels, were blunted by ramipril or losartan treatment. Hypertrophic regression was associated with reduced mortality in rats treated with ramipril (11%) and losartan (13%) versus hydralazine (20%) and vehicle (31%). Thus, the renin-angiotensin system may be involved in the maintenance of chronic left ventricular hypertrophy. Blockade of the system may result in regression of the hypertrophic phenotype and improve survival in rats despite persistent pressure overload.
Hypertension 1995 Feb
PMID:Blockade of the renin-angiotensin system in cardiac pressure-overload hypertrophy in rats. 784 75

The changes in myocardial contractility and ventricular myosin isoenzymes were investigated in rats with pressure-overload cardiac hypertrophy as well as during its regression. Hypertrophic myocardium was obtained from rats with renovascular hypertension (Goldblatt rats), rats with abdominal aortic constriction (AC), and spontaneously hypertensive rats (SHR). Regression of cardiac hypertrophy was induced by lowering the blood pressure through nephrectomy on the affected side in Goldblatt rats, by opening the clip which constricted the abdominal aorta in AC rats, and by the administration of antihypertensive agents to SHR. The isometric developed tension of isolated left ventricular papillary muscles and the maximum rate of increase in the tension (dT/dtmax) were measured. Left ventricular myosin isoenzymes were separated by pyrophosphate gel electrophoresis. Isometric developed tension remained unchanged, but dT/dtmax was decreased in hypertrophic myocardium, although it recovered along with the regression of cardiac hypertrophy. The left ventricular myosin isoenzyme pattern was shifted towards V3 in hypertrophic myocardium, and shifted back again towards V1 with the regression of cardiac hypertrophy. These results indicate that relief of hemodynamic overload is one of the most important elements in the regression of cardiac hypertrophy and the associated physiological or biochemical alterations. However, other factors such as neurohumoral influences must also be taken into consideration.
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PMID:Myocardial contractility and energetics in cardiac hypertrophy and its regression. 817 35

Intracellular pH is under strict control in myocardium; H+ are extruded from the cells by sodium-dependent mechanisms, mainly Na+/H+ exchanger and Na+/HCO3- symport, whereas Na+-independent Cl-/HCO3- exchanger extrudes bases on intracellular alkalinization. Hypertrophic myocardium from spontaneously hypertensive rats (SHR) exhibits increased Na+/H+ exchange activity that is accompanied by enhanced extrusion of bases through Na+-independent Cl-/HCO3- exchange. The present experiments were designed to investigate the effect of enalapril-induced regression of cardiac hypertrophy on the activity of these exchangers. Male SHR and normotensive Wistar-Kyoto rats (WKY) received enalapril maleate (20 mg/kg per day) in the drinking water for 5 weeks. Gender- and age-matched SHR and WKY were used as untreated controls. Enalapril treatment significantly reduced systolic blood pressure in SHR and completely regressed cardiac hypertrophy. Na+/H+ activity was estimated in terms of both steady pHi value in HEPES buffer and the rate of pHi recovery from CO2-induced acid load. Na+-independent Cl-/HCO3- activity was assessed by measuring the rate of pHi recovery from intracellular alkalinization produced by trimethylamine exposure. Regression of cardiac hypertrophy was accompanied by normalization of Na+/H+ and Na+-independent Cl-/HCO3- exchange activities. Inhibition of protein kinase C (PKC) activity with chelerythrine (10 mmol/L) or calphostin C (50 nmol/L) returned both exchange activities to normal values. These results show that angiotensin-converting enzyme inhibition normalizes the enhanced activity of both exchangers while regressing cardiac hypertrophy. Because normalization of exchange activities could be also achieved by PKC inhibition, the data would suggest that PKC-dependent mechanisms play a significant role in the increased ion exchange activities of hypertrophic myocardium and in their normalization by angiotensin-converting enzyme inhibition.
Hypertension 1998 Apr
PMID:Enalapril induces regression of cardiac hypertrophy and normalization of pHi regulatory mechanisms. 953 21

Vascular structure, function, and mechanics are altered in hypertension, which contributes to an important degree to complications of elevated blood pressure. Vascular hypertrophy with collagen deposition and increased stiffness is found in large arteries, whereas in small arteries, smooth muscle cells are restructured around a smaller lumen, and there is no net growth of the vascular wall, particularly in milder forms of hypertension. Hypertrophic remodeling and increased small artery stiffness may be found in more severe hypertension. Endothelial dysfunction occurs in large or smaller vessels in a variable percentage of patients, particularly in presence of other risk factors such as diabetes, smoking, dyslipidemia, and advanced atherosclerosis. In clinical trials, 1-year treatment with angiotensin-converting enzyme inhibitors, angiotensin AT1 receptor antagonists, and long-acting calcium channel blockers corrected small artery structure and endothelial dysfunction in hypertensive patients, whereas beta-adrenergic receptor blockers did not. Improved outcomes in hypertensive patients demonstrated in recent trials with some but not others of these agents could be a consequence, at least in part, of vascular protection offered by some antihypertensive agents.
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PMID:Small artery remodeling in hypertension: can it be corrected? 1146 50

Blood vessels are remodeled in hypertension both structurally and functionally. The changes that occur in their structure, mechanical properties, and function contribute to blood pressure elevation and to complications of hypertension. We studied the remodeling of small arteries in experimental animals and humans. Smooth muscle cells of small arteries are restructured around a smaller lumen, with significant remodeling of the extracellular matrix and collagen and fibronectin deposition. Interestingly, there is no evidence of net growth of the vascular wall (which results in so-called eutrophic remodeling), particularly in the milder forms of human essential hypertension. Hypertrophic remodeling and increased small artery stiffness may be found in more severe forms of hypertension. Almost all hypertensive patients have vascular structural remodeling. However, only some exhibit endothelial dysfunction. This is particularly true in mild hypertension, in which endothelial dysfunction is less common. A 1-year treatment of hypertensive patients with angiotensin converting enzyme inhibitors, angiotensin AT1 receptor antagonists, and long acting calcium channel blockers corrected small artery structure and, to variable degrees depending on the agents used, impaired endothelial function. In contrast, beta blockers did not improve structure, function, or mechanics of vessels. When beta-blocker-treated patients were switched to an AT1 receptor antagonist, small artery structure and impaired endothelial function were corrected. The vascular protective action of some antihypertensive agents may contribute to improve outcome for hypertensive patients, although this is presently unproven.
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PMID:Effect of antihypertensive treatment on small artery remodeling in hypertension. 1271 May 31

In this lecture, I attempted to demonstrate MR imaging of the cerebral tracts, medullospinal junction and spinal cord. Cortical migration disorders includes heterotopic gray matter, pachygyria and polymicrogyria. Delayed myelination and dysmyelination are shown as hyper signal intensity in the white matter on T2-weighted images. Edema and demyelination impair the tracts, and they are precisely evaluated by T2-weighted, FLAIR and diffusion-weighted MR images. Reversible posterior leukoencepalopaty syndrome is caused by vasogenic edema of the subcortical association fibers and by cytotoxic edema of the cortical gray matter, due to hypertension, renal dysfunction, drugs and so on. Antiepileptic drug toxicity may cause reversible edema of the splenium. Secondary demyelination includes Wallerian degeneration and transneuronal degeneration. Hypertrophic olivery degeneration is transneuronal degeneration associated with disruption of Guillain-Mollaret's triangle, and it is shown as high signal intensity of the inferior olivery nucleus on T2 and FLAIR images. Limbic system and Papez's circuit play an important role in epilepsy associated with mesial temporal sclerosis. Transneuronal degeneration through the Papez's circuit can be appreciated by the findings of atrophy of the fornix and mammillary body.
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PMID:[Diagnostic imaging of the CNS disorders]. 1278 73

We have previously reported a quantitative trait locus associated with pressure-independent cardiac hypertrophy in the spontaneously hypertensive rat (SHR) of the Okamoto strain. This locus (Lvm1; left ventricular mass locus 1) contains the gene Fgf2 that codes for the potent cardiac growth factor, Fibroblast Growth Factor 2 (FGF2). Given that FGF2 appears essential for the induction of certain forms of cardiac hypertrophy in the rat, we proposed this gene as a candidate for the cardiac enlargement seen in the SHR. Previous reports of elevated FGF2 mRNA levels in the SHR, led us to hypothesise that nucleotide sequence variations occurring in the coding regions or in putative transcriptional factor binding sites within the Fgf2 promoter might play a role in cardiac hypertrophy in this strain. Given that we have also recently derived from the SHR a rat strain that develops spontaneous cardiac hypertrophy in the absence of hypertension (the Hypertrophic Heart Rat; HHR), we also took the opportunity to examine the sequence of its Fgf2 promoter and coding region. However, extensive sequence analysis of the promoter and coding regions of the SHR and HHR Fgf2 genes failed to reveal any nucleotide variations between strains. Thus, we conclude that variations in the nucleotide sequence of the promoter and coding region of the SHR Fgf2 gene do not play a role in the cardiac hypertrophy of the SHR and HHR strains.
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PMID:Sequence analysis of the fibroblast growth factor 2 gene from the spontaneously hypertensive and hypertrophic heart rats. 1513 99


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