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)

Contemplation of non-genetic risk factors that are influencing the onset and development of diabetic nephropathy (diabetic kidney disease--DKD) is very important. This article is integrative, assessing the existent data about several possible risk factors for DKD. Because the age of onset and postpubertal duration of diabetes seems to be strongly correlated with DKD, it is feasible for puberty to be another independent risk factor. Data analysis regarding puberty and possible explanatory mechanisms to link it with DKD, as the connection with DKD of other situations, with special hormonal status (like pregnancy), is also part of this article. Summing up the data about hormonal status, we can conclude that ANF levels are a risk factor for diabetic nephropathy because they are implicated in diminution of urinary Na elimination and hypertension and subsequent urinary albumin excretion (UAE) in case of inadequate glycaemic control. The evidences regarding GH are indicating that it is a risk factor for DKD and that he is probably implicated in glomerular hypertrophy onset at puberty. The urinary elimination levels of GH are very strong correlated with UAE being putative early marker for DKD. Also the GH deficiency seems to be a protective mechanism for DKD apparition. GH is strongly correlated with IGF-1 that has very high urinary levels in microalbuminuric patients. These levels are very well related to UAE, kidney volume--important markers for glomerular hypertrophy. The evidences accumulated until now regarding the role of masculine gender, testosterone and estrogens in DKD are inarticulate.
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PMID:[Puberty, pregnancy, gender and hormonal status--putative risk factors for diabetic nephropathy]. 2149 93

ANF-RGC is the prototype membrane guanylate cyclase, both the receptor and the signal transducer of the hormones ANF and BNP. After binding them at the extracellular domain, it, at its intracellular domain, signals activation of the C-terminal catalytic module and accelerates production of the second messenger, cyclic GMP. This, in turn, controls the physiological processes of blood pressure, cardiovascular function, fluid secretion, and others: metabolic syndrome, obesity, and apoptosis. The biochemical mechanism by which this single molecule controls these diverse processes, explicitly blood pressure regulation, is the subject of this study. In line with the concept that the structural modules of ANF-RGC are designed to respond to more than one yet distinctive signals, the study demonstrates the construction of a novel ANF-RGC-In-gene-(669)WTAPELL(675) mouse model. Through this model, the study establishes that (669)WTAPELL(675) is a vital ANF signal transducer motif of the guanylate cyclase. Its striking physiological features linked with their biochemistry are the following. (1) It controls the hormonally dependent cyclic GMP production in the kidney and the adrenal gland. Its deletion causes (2) hypertension and (3) cardiac hypertrophy. (4) These mice show higher levels of the plasma aldosterone. For the first time, a mere seven-amino acid-encoded motif of the mouse gene has been directly linked with the physiological control of blood pressure regulation, a detailed biochemistry of this linkage has been established, and a model for this linkage has been described.
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PMID:The ANF-RGC gene motif (669)WTAPELL(675) is vital for blood pressure regulation: biochemical mechanism. 2346 24


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