Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors retrospectively analyzed the prevalence of renal artery stenosis in 63 consecutive patients with aortic dissection who underwent thoracic and abdominal aortography. Ten patients (16%) had renal artery stenosis, five with atherosclerosis and five with fibromuscular lesions. Risk factors for aortic dissection were Marfan disease in nine patients, bicuspid aortic valve in one, and hypertension in 54 (including seven patients with Marfan syndrome). If the patients with Marfan syndrome and the patient with the bicuspid aortic valve are excluded, renal artery stenosis was present in 10 of 53 patients (19%) when the cause of dissection was presumably hypertension. This finding suggests that renovascular hypertension is a greater risk factor for aortic dissection than is essential hypertension. The success of angiotensin converting enzyme inhibitors and percutaneous transluminal renal angioplasty (PTRA) in controlling renovascular hypertension has been proved. In this series, emergent PTRA successfully controlled the hypertension in one patient with a type B dissection, resulting in an excellent clinical outcome. Angiography should be routinely performed on patients with aortic dissections to evaluate for renal artery stenosis.
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PMID:Renal artery stenosis in patients with aortic dissection: increased prevalence. 205 16

Atherosclerosis is characterized by inflammatory metabolic change with lipid accumulation in the artery. Atherosclerotic plaque occurs at discrete locations in the arterial system and involves the proliferation of smooth muscle cells (SMCs) together with imbalance of the extracellular matrix elements, elastic fiber in particular. The role of elastin in arterial development and disease was confirmed by generating mice that lack elastin. Thus, elastin is a critical regulatory molecule that regulates the phenotypic modulation, proliferation and migration of SMCs. We estimated that elastin expression and SMC proliferation are coupled inversely: potent stimulators of cell proliferation may potentially inhibit elastin expression and potent inhibitors of cell proliferation can stimulate elastin expression. Moreover, elastin was found to be expressed maximally at the G(0) and minimally at the G(2)/M phase during the cell cycle, suggesting that its expression is regulated by the cell growth state. The elastin peptide VPGVG enhanced SMC proliferation, resulting in the reduction of elastin expression. The inhibition of elastin expression by elastin fragments may be reflected in the negative feedback regulatory mechanism. The relationship between cell proliferation and elastin expression may be changed in atherosclerosis. Areas of atherosclerotic plaque show abnormality of elasticity and permeability from the viewpoint of the physiological function of the arterial wall. The etiology was estimated to be that cholesterol and calcium are deposited on the elastic fiber, resulting in decreased elastin synthesis and cross-linking formation. In addition, these dysfunctions of elastin fiber are also associated, in that the down-regulation of elastin and its related components (fibrillin-1 and lysyl oxidase) are directly related to calcification in SMCs. The denatured arterial elastin by cholesterol and calcium accumulation was also susceptible to proteolytic enzymes such as elastase and matrix metalloproteinase (MMP). Therefore, metabolic change in elastic fiber induces decreased elasticity and is associated with essential hypertension. Vitamin K(2) is used in drug therapy against atherosclerosis, or calcification in diabetes mellitus or dialysis, due to its promotion of the carboxylation of the matrix Gla protein.
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PMID:Atherosclerosis and matrix dystrophy. 1555 5