BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: E Gavriilaki; E Gkaliagkousi; B Nikolaidou; G Triantafyllou; F Chatzopoulou; S Douma Journal: J Hum Hypertens Date: 2014-03-13 Impact factor: 3.012