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)

Hypertension is an important health problem that is manifested by systemic arterial blood pressure being permanently elevated and leading to serious complications. Hypertension is the basis for coronary heart diseases, heart failure, kidney damage, cerebrovascular diseases. Due to ethical concerns, there is no detailed study of the mechanism, side effects and treatment of hypertension in humans. For this reason, specific studies related to the organ of hypertension are performed in experimental animals. The heart and kidney tissue, which are the most important organs that hypertension has damaged, have formed specific organs of our work. In our experimental study, a total of 35 (hypertensive group: 20, control group: 15) Rattus Norvegicus Wistar albino rats were used. In order to obtain our hypertension model, our experimental animals were given L-NAME together with drinking water for six weeks. After six weeks, the experimental procedures were terminated. Heart and kidney tissues of the hypertensive and control group were obtained. Expression of apelin and apelin receptor (APJ) was demonstrated by immunohistochemical and Western Blot protocols. Hypertrophic cardiac atrium of the hearts of the large cavities, interventricular septum and myocardium to the disintegration, as well as an increase in the diameter of the coronary artery has been observed. In general, kidney tissues of the hypertensive group showed narrowing in cortical renal structures and enlargement in structures in the renal medulla. As a result, in hypertensive cases, there was an increase in expression of Apelin and APJ receptor in heart tissue, and a decrease in expression of Apelin and APJ receptor in kidney tissue. We think that our findings may contribute to experimental or clinical studies related to hypertension and apelin.
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PMID:Apelin/APJ expression in the heart and kidneys of hypertensive rats. 2939 16

Hypertrophic cardiomyopathies represent a heterogeneous group of pathophysiological mechanisms and etiologies (genetic or not), which lead to the development of left ventricular hypertrophy. Left ventricular hypertrophy, when not explained by a significant and prolonged increase in post-load (such as severe poorly controlled arterial hypertension or severe aortic stenosis) justifies etiological exploration. The etiology may range from physiological adaptation in the athlete to myocardial involvement, isolated or integrated as part of a global neuromuscular involvement; metabolic or mitochondrial disease to deposition disease. As cardiac signs are non-specific, the clinical examination should focus on looking for a syndromic entity. Considering this pathophysiological heterogeneity, in addition to the biological assays in search of a metabolic or infiltrative cause, the minimum check-up must include an electrocardiogram and a transthoracic echocardiography, which will most of the time be completed by magnetic resonance imaging, and even bone scintigraphy in the event of suspected amyloidosis. The question of genetic analysis and/or counselling should be systematically considered. The treatment is mainly symptomatic, aimed at controlling congestive signs and/or intraventricular obstruction, with the exception of amyloidosis and Fabry disease for which dedicated treatments have been developed. The rhythmic risk must be evaluated and can justify the implantation of an automatic defibrillator.
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PMID:[Hypertrophic cardiomyopathies]. 3073 54


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