共查询到20条相似文献,搜索用时 31 毫秒
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M. J. Brown 《BMJ (Clinical research ed.)》1997,314(7089):1258-1261
The abundance of drugs now available for treating hypertension, and evidence that small reductions in blood pressure reverse the associated risk of stroke have shifted clinical concerns away from hypertension. However, we do not understand the cause of hypertension in 95% of patients, fail to achieve a normal blood pressure in 50% of patients, and are unable fully to reverse the cardiac and vascular changes that predate the diagnosis and treatment of hypertension. Consequently, hypertension remains the commonest cause of strokes in Britain and of renal failure in the United States. Essential hypertension is a polygenic disease whose understanding can now be advanced through molecular genetic analyses. Several different syndromes are likely to be recognised; most will be due to interactions between genetic and environmental factors, but there are also likely to be further monogenic syndromes in families with multiple affected members. Recognition of these syndromes will permit accurate genetic prediction of prognosis and optimal treatment and perhaps lead to new and more powerful classes of antihypertensive treatment. 相似文献
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S. Krishna 《BMJ (Clinical research ed.)》1997,315(7110):730-732
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S. J. Russell 《BMJ (Clinical research ed.)》1997,315(7118):1289-1292
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J. Wilding 《BMJ (Clinical research ed.)》1997,315(7114):997-1000
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Prostaglandins are part of the family of oxygenated metabolites of arachidonic acid known collectively as eicosanoids. While they are formed, act, and are inactivated locally and rarely circulate in plasma, they can affect blood flow in some tissues and so might contribute to the control of peripheral vascular resistance. Few studies have shown any derangement of total body prostaglandin synthesis or metabolism in hypertension, but increased renal synthesis of one prostanoid, thromboxane A2, has been noted in spontaneously hypertensive rats and some hypertensive humans. This potent vasoconstrictor may account for the increased renal vascular resistance and suppressed plasma renin activity seen in many patients with hypertension. Increased renal vascular resistance could increase the blood pressure directly as a component of total peripheral resistance or indirectly by increasing glomerular filtration fraction and tubular sodium reabsorption. Specific thromboxane synthesis inhibitors not only decrease renal thromboxane production but also increase renal vasodilator prostaglandin synthesis when prostaglandin synthesis is stimulated. This redirection of renal prostaglandin synthesis toward prostacyclin might be of benefit in correcting a fundamental renal defect in patients with hypertension. 相似文献
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E Rapaport 《The Western journal of medicine》1989,151(5):551-552
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S D Henriksen 《Microbiological reviews》1973,37(4):522-561
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