2nd Propedeutic Department of Internal Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Am J Hypertens. 2014 Apr;27(4):571-8. doi: 10.1093/ajh/hpt153. Epub 2013 Aug 23.
Acute exercise may exert deleterious effects on the cardiovascular system through a variety of pathophysiological mechanisms, including increased platelet activation. However, the degree of exercise-induced platelet activation in untreated hypertensive (UH) individuals as compared with normotensive (NT) individuals has yet to be established. Furthermore, the effect of antihypertensive treatment on exercise-induced platelet activation in essential hypertension (EH) remains unknown.
Study 1 consisted of 30 UH and 15 NT subjects. UH subjects who received treatment were included in study 2 and were followed-up after a 3-month treatment period with an angiotensin II receptor blocker (ARB; valsartan). Circulating monocyte-platelet aggregates (MPA) and platelet P-selectin were measured as platelet activation markers at baseline, immediately after a treadmill exercise test, and 10, 30, and 90 minutes later.
Maximal platelet activation was observed at 10 minutes after peak exercise in both groups. In UH subjects, MPA levels remained increased at 30 minutes after peak exercise, despite BP fall to baseline levels. MPA levels were significantly higher in UH subjects than NT subjects at maximal exercise and at 10 and 30 minutes of recovery. Post-treatment MPA levels increased significantly only at 10 minutes into recovery and were similar to those of NT subjects.
Acute high-intensity exercise exaggerates platelet activation in untreated patients with EH compared with NT individuals. Angiotensin II receptor blockade with adequate BP control greatly improves exercise-induced platelet activation in EH. Further studies are needed to clarify whether this phenomenon depends purely on BP lowering or benefits also from the pleiotropic effects of ARBs.
急性运动通过多种病理生理机制对心血管系统产生有害影响，包括血小板激活增加。然而，未经治疗的高血压（UH）个体与正常血压（NT）个体相比，运动引起的血小板激活程度尚未确定。此外，在原发性高血压（EH）中，抗高血压治疗对运动引起的血小板激活的影响尚不清楚。
研究 1 包括 30 名 UH 和 15 名 NT 受试者。接受治疗的 UH 受试者被纳入研究 2，并在接受血管紧张素 II 受体阻滞剂（ARB；缬沙坦）治疗 3 个月后进行随访。在基线、跑步机运动测试后即刻以及 10、30 和 90 分钟后，测量循环单核细胞-血小板聚集物（MPA）和血小板 P-选择素作为血小板激活标志物。
在两组中，最大血小板激活都发生在峰值运动后 10 分钟。在 UH 受试者中，尽管血压降至基线水平，但 MPA 水平在峰值运动后 30 分钟仍保持升高。在最大运动和恢复的 10 和 30 分钟时，UH 受试者的 MPA 水平明显高于 NT 受试者。治疗后 MPA 水平仅在恢复的 10 分钟内显著增加，与 NT 受试者相似。
与 NT 个体相比，未经治疗的 EH 患者在急性高强度运动时会加剧血小板激活。用充分的血压控制进行血管紧张素 II 受体阻断可显著改善 EH 患者的运动诱导的血小板激活。需要进一步研究来阐明这种现象是否仅取决于降压作用，还是也受益于 ARB 的多效作用。
