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前列腺素在人类高血压中的作用。

The role of prostaglandins in human hypertension.

作者信息

Smith M C, Dunn M J

出版信息

Am J Kidney Dis. 1985 Apr;5(4):A32-9. doi: 10.1016/s0272-6386(85)80063-9.

Abstract

A large body of evidence supports the concept that prostaglandins (PG) are importantly involved in arterial pressure regulation. Various PGs, especially PGE2 and prostacyclin (PGI2) may influence blood pressure through control of vascular tone, sodium excretion, and renin release. Inhibition of PG synthesis by nonsteroidal antiinflammatory drugs (NSAID) augments the vasoconstrictor response to exogenous pressors such as angiotensin II, arginine vasopressin (AVP), and fludrocortisone. The acute administration of NSAID to either normotensive or untreated hypertensive subjects results in an increase in arterial pressure and peripheral resistance; long-term administration, however, is associated with little or no change in blood pressure, possibly because of a reduction in cardiac output. Although NSAID have little influence on blood pressure in normotensive subjects or untreated hypertensives, inhibition of PG synthesis blunts or abolishes the antihypertensive effect of most antihypertensive agents. NSAID antagonize the vasodepressor action of diuretics, beta-adrenoreceptor antagonists, vasodilators, and converting enzyme inhibitors. Consequently, potent NSAID should be used with caution, if at all, during treatment of hypertensive patients. Numerous studies have examined renal PG production in essential hypertension (EH). The majority have demonstrated reduced basal and stimulated urinary PGE2 excretion in EH compared to normotensive subjects, but there is substantial overlap. Nevertheless, renal PGE2 synthesis is significantly decreased in approximately one-third of patients with EH. A recent innovative approach to arterial pressure regulation has focused on dietary supplementation with polyunsaturated fatty acids (PUFA), especially linoleic acid and eicosapentaenoic acid. Several groups have demonstrated that long-term dietary supplementation with PUFA reduces blood pressure in both normotensive individuals and in patients with EH.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

大量证据支持前列腺素(PG)在动脉血压调节中起重要作用这一概念。各种PG,尤其是前列腺素E2(PGE2)和前列环素(PGI2),可能通过控制血管张力、钠排泄和肾素释放来影响血压。非甾体抗炎药(NSAID)抑制PG合成会增强对外源性升压药如血管紧张素II、精氨酸加压素(AVP)和氟氢可的松的血管收缩反应。对血压正常或未经治疗的高血压患者急性给予NSAID会导致动脉血压和外周阻力升高;然而,长期给药与血压几乎没有变化相关,这可能是由于心输出量减少。虽然NSAID对血压正常的个体或未经治疗的高血压患者的血压影响很小,但抑制PG合成会减弱或消除大多数抗高血压药物的降压作用。NSAID拮抗利尿剂、β-肾上腺素能受体拮抗剂、血管扩张剂和转换酶抑制剂的血管舒张作用。因此,在治疗高血压患者时,强效NSAID即使使用也应谨慎。许多研究已经检查了原发性高血压(EH)患者的肾脏PG生成。大多数研究表明,与血压正常的受试者相比,EH患者基础和刺激后的尿PGE2排泄减少,但存在很大重叠。尽管如此,大约三分之一的EH患者肾脏PGE2合成明显减少。最近一种创新的动脉血压调节方法集中在饮食中补充多不饱和脂肪酸(PUFA),尤其是亚油酸和二十碳五烯酸。几个研究小组已经证明,长期饮食中补充PUFA可降低血压正常个体和EH患者的血压。(摘要截短于250字)

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