de Leeuw P W
Department of Medicine, University Hospital Maastricht, Netherlands.
Drugs. 1996 Feb;51(2):179-87. doi: 10.2165/00003495-199651020-00001.
Prostaglandins play an important role in cardiovascular homeostasis. Among other things, they promote vasodilation and enhance sodium excretion. Since they act as local hormones, it is difficult to assess their activity in the intact organism. Nonsteroidal anti-inflammatory drugs (NSAIDs) block the synthesis of prostaglandins, and thus may interfere with circulatory control. Indeed, many reports show that blood pressure may rise during treatment with one of these drugs. However, meta-analyses of such reports indicate that the rise in mean arterial pressure is relatively small, being approximately 5 mm Hg. At the present time, it is not known whether this confers any risk in terms of cardiovascular complications. Moreover, the trials on which this information is based are of relatively short duration. Whether the increment in blood pressure following administration of NSAIDs is sustained over time has not been established. Also, there is insufficient information regarding whether there are any special subgroups in the population who are at risk of developing hypertension during exposure to NSAIDs. Some data suggest that elderly people and patients with pre-existing hypertension carry an increased risk, notably when they are receiving antihypertensive treatment. Available data suggest that not all NSAIDs are equal as far as their effect on blood pressure is concerned. Sulindac, and perhaps also aspirin, seem to be less troublesome in this respect than other NSAIDs. This also applies to their effects on the kidney. Unfortunately, the mechanisms whereby NSAIDs may raise blood pressure are not fully understood. Interference with both the control of vascular resistance and the regulation of extracellular volume homeostasis has been incriminated, but several other putative mechanisms such as moderation of adrenergic activity or resetting of the baroreceptor response may also be involved. For the practising physician, it is wise to balance the risk of an increase in blood pressure against the expected benefit of treatment with an NSAID. In patients with (treated) hypertension and in the elderly, the benefits may not always outweigh the admittedly small risk. Should the physician nevertheless decide to prescribe an NSAID, frequent measurement of blood pressure may be necessary during the first weeks of treatment.
前列腺素在心血管稳态中发挥着重要作用。它们除了其他作用外，还能促进血管舒张并增强钠排泄。由于它们作为局部激素起作用，因此很难评估它们在完整机体中的活性。非甾体抗炎药（NSAIDs）会阻断前列腺素的合成，从而可能干扰循环控制。事实上，许多报告表明，使用这些药物之一进行治疗期间血压可能会升高。然而，对此类报告的荟萃分析表明，平均动脉压的升高相对较小，约为5毫米汞柱。目前，尚不清楚这是否会带来任何心血管并发症方面的风险。此外，这些信息所基于的试验持续时间相对较短。服用NSAIDs后血压升高是否会随时间持续尚未确定。而且，关于人群中是否存在任何在接触NSAIDs期间有患高血压风险的特殊亚组，目前信息不足。一些数据表明，老年人和已有高血压的患者风险增加，特别是在他们接受抗高血压治疗时。现有数据表明，就其对血压的影响而言，并非所有NSAIDs都是相同的。舒林酸，或许还有阿司匹林，在这方面似乎比其他NSAIDs麻烦更少。这也适用于它们对肾脏的影响。不幸的是，NSAIDs可能升高血压的机制尚未完全理解。血管阻力控制和细胞外液量稳态调节均受到干扰，但也可能涉及其他一些假定机制，如肾上腺素能活性的调节或压力感受器反应的重置。对于执业医生来说，明智的做法是权衡血压升高的风险与使用NSAIDs治疗预期的益处。在（接受治疗的）高血压患者和老年人中，益处可能并不总是超过公认的小风险。然而，如果医生仍然决定开NSAIDs处方，在治疗的头几周可能需要频繁测量血压。
