Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004135 (ATM)
 13,001 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from patients with malignant essential hypertension (n = 14), malignant secondary hypertension mainly attributable to renovascular diseases (n = 12) and renovascular diseases without malignant hypertension (n = 11) and from normotensive healthy blood donors (n = 35) were studied for the presence of autoantibodies against G-protein-coupled cardiovascular receptors. Autoantibodies against the angiotensin II receptor (AT1) were detected in 14, 33, 18 and 14% of patients with malignant essential hypertension, malignant secondary hypertension, renovascular diseases and control patients, respectively. Sensitivity of the enzyme immunoassay was assessed as 5 microg/ml IgG. Patients did not show antibodies against bradykinin (B2) or angiotensin II subtype 2 (AT2) receptors. Autoantibodies affinity-purified from positive patients localized AT receptors in Chinese hamster ovary transfected cells, and displayed a positive chronotropic effect on cultured neonatal rat cardiomyocytes. These results demonstrate the existence of autoantibodies against a functional extracellular domain of human AT1 receptors in patients with malignant hypertension, and suggest that these autoantibodies might be involved in the pathogenesis of malignant hypertension.
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PMID:Autoantibodies against the angiotensin receptor (AT1) in patients with hypertension. 1093 Jan 93

It has been clearly demonstrated that left ventricular (LV) hypertrophy is a strong blood pressure independent risk factor for cardiovascular morbidity and mortality in the general population, in primary and secondary hypertension and in cardiac patients. LV hypertrophy in arterial hypertension develops in response to an increased afterload, but underlying pathophysiological mechanisms include a variety of non-haemodynamic factors. Due to the prognostic importance of LV hypertrophy, normalisation of LV mass emerged as a desirable goal of antihypertensive treatment. Indeed, several prospective studies now indicate that regression of LV hypertrophy reduced cardiovascular complications. As a consequence, the question was raised whether certain antihypertensive drugs differ in their ability to reduce LV mass. Several comparative studies and meta-analyses have been carried out to resolve this issue. The available data seem to indicate that angiotensin-converting enzyme (ACE)-inhibitors and calcium channel blockers were more potent than beta-blockers in their ability to reduce LV hypertrophy, with diuretics in the intermediate range. The role of new antihypertensive agents such as angiotensin II AT1-receptor blockers appears similar to the one of ACE-inhibitors, since in some studies angiotensin II AT1-receptor blockers were superior to beta-blockers and diuretics. Various aspects of LV hypertrophy including its prevalence, determinants, prognosis and regression are discussed in this article.
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PMID:Hypertension and the heart. 1109 53

In transgenic hypertensive TGR(mREN2)27 rats (TGR) harboring the murine Ren-2 gene an inverse 24h blood pressure (BP) profile was described in relation to a normal pattern in heart rate (HR) and motility (MA), normotensive Sprague-Dawley rats (SDR) were used as controls. Transgenic rats as an animal model of human secondary hypertension (non-dipper) was studied in detail at different levels: (1) Radiotelemetry was applied to document gross circadian rhythms/rhythm disturbances in cardiovascular functions, MA and body temperature under normal LD conditions, under DD and after a light pulse. (2) Signal transduction of the overexpressed renin-angiotensin in TGR was studied by determation of AT1-receptors in kidney glomeruli together with kidney functions. (3) Expression of key processes involved in increased sympathetic regulation in TGR, mRNAs, the tyrosine-hydroxylase (TH) and norepinephrine (NE) reuptake1-carrier were determined. (4) In the SCN mRNA of c-fos and c-jun were determined under LD and after light pulse. (5) In primary cultures of pinealocytes the effects of adrenergic agonists and antagonists were evaluated on second messenger (cAMP, cGMP) accumulation and melatonin release. The results of these studies clearly demonstrate that the additional mouse renin genin in TGR greatly affected not only the renin-angiotensin-system and led--as expected--to an increased BP in this rat but also disturbed circadian rhythms from the BP pattern down to the level of hormones, processes of signal transduction, and expression of transcription factors and clock genes. In conclusion, the expression of a single additional gene is able to disturb the circadian system of an animal in a highly complex way. These findings are importance for chronobiologic as well as pharmacologic research.
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PMID:Transgenic TGR(mREN2)27 rats as a model for disturbed circadian organization at the level of the brain, the heart, and the kidneys. 1291 22

Arterial hypertension is the most common internal disorder. Therefore, rational strategies in diagnostic and therapeutic procedures are especially important. In the diagnosis of hypertension, basic and special diagnostic procedures are established, the former being restricted to few procedures. Basic diagnostic procedures should be applied to any patient with hypertension. Special diagnostic procedures should only be applied if basic procedures show abnormalities, if patients are resistant to conventional treatment or show any other signs suggestive of secondary hypertension. The basis of drug treatment consists of the following first line antihypertensive drugs: diuretics, beta blockers, calcium channel blockers, ACE inhibitors, and AT1 blockers. Differential therapy is based on the condition of the individual patient. Rational treatment strategies include stepped care, initial low-dose combination therapy, and sequential monotherapy.
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PMID:[Novel guidelines for antihypertensive treatment. Proven and new]. 1583 71

Hypertension is a disease classified as primary or secondary, manifested not only by elevation of blood pressure but also involved in structural and functional changes of target organs. Renal artery stenosis is a leading factor of secondary hypertension, and its progress is associated with overactivation of the renin-angiotensin-aldosterone system (RAAS). Aliskiren is a renin inhibiting drug that suppresses RAAS and culminates in decreased renin release, plasma angiotensin II concentration, and inhibition of aldosterone secretion. In this sense, the aim of the present study was to analyze the structural and ultrastructural morphophysiology of the adrenal glomerular zone, after treatment with aliskiren in Wistar rats with 2K1C hypertension. Parameters as structure and ultrastructure of the adrenal glomerular zone, cellular apoptosis, nuclear cell proliferation, and AT1 receptor expression were analyzed by immunostaining and electron microscopy. Our results showed that the hypertensive animals treated with aliskiren presented a reestablishment of AT1 receptor expression and decrease in apoptosis and autophagy. In addition, treatment with aliskiren improves the cell aspects in the adrenal glomerular zone, evidenced by ultrastructural analysis through preserved nuclei and well-developed mitochondria. Therefore, our evidence suggests that aliskiren has a beneficial effect on the adrenal glomerular zone remodeling in animals with renovascular hypertension.
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PMID:Aliskiren Reduces the Adrenal Zona Glomerulosa Apoptosis and Autophagy in Wistar Rats with 2K1C Hypertension. 3314 9