Exercise training alters the balance between vasoactive compounds in skeletal muscle of individuals with essential hypertension

TY - JOUR

T1 - Exercise training alters the balance between vasoactive compounds in skeletal muscle of individuals with essential hypertension

AU - Hansen, Ane Håkansson

AU - Nyberg, Michael Permin

AU - Bangsbo, Jens

AU - Saltin, Bengt

AU - Hellsten, Ylva

N1 - CURIS 2011 5200 089

PY - 2011/11

Y1 - 2011/11

N2 - The effects of physical training on the formation of vasodilating and vasoconstricting compounds, as well as on related proteins important for vascular function, were examined in skeletal muscle of individuals with essential hypertension (n=10). Muscle microdialysis samples were obtained from subjects with hypertension before and after 16 weeks of physical training. Muscle dialysates were analyzed for thromboxane A 2, prostacyclin, nucleotides, and nitrite/nitrate. Protein levels of thromboxane synthase, prostacyclin synthase, cyclooxygenase 1 and 2, endothelial nitric oxide synthase (eNOS), cystathionine-γ-lyase, cytochrome P450 4A and 2C9, and the purinergic receptors P2X1 and P2Y2 were determined in skeletal muscle. The protein levels were compared with those of normotensive control subjects (n=12). Resting muscle dialysate thromboxane A 2 and prostacyclin concentrations were lower (P<0.05) after training compared with before training. Before training, dialysate thromboxane A 2 decreased with acute exercise, whereas after training, no changes were found. Before training, dialysate prostacyclin levels did not increase with acute exercise, whereas after training there was an 82% (P<0.05) increase from rest to exercise. The exercise-induced increase in ATP and ADP was markedly reduced after training (P<0.05). The amount of eNOS protein in the hypertensive subjects was 40% lower (P<0.05) than in the normotensive control subjects, whereas cystathionine-γ-lyase levels were 25% higher (P<0.05), potentially compensating for the lower eNOS level. We conclude that exercise training alters the balance between vasodilating and vasoconstricting compounds as evidenced by a decrease in the level of thromboxane, reduction in the exercise-induced increase in ATP and a greater exercise-induced increase in prostacyclin.

AB - The effects of physical training on the formation of vasodilating and vasoconstricting compounds, as well as on related proteins important for vascular function, were examined in skeletal muscle of individuals with essential hypertension (n=10). Muscle microdialysis samples were obtained from subjects with hypertension before and after 16 weeks of physical training. Muscle dialysates were analyzed for thromboxane A 2, prostacyclin, nucleotides, and nitrite/nitrate. Protein levels of thromboxane synthase, prostacyclin synthase, cyclooxygenase 1 and 2, endothelial nitric oxide synthase (eNOS), cystathionine-γ-lyase, cytochrome P450 4A and 2C9, and the purinergic receptors P2X1 and P2Y2 were determined in skeletal muscle. The protein levels were compared with those of normotensive control subjects (n=12). Resting muscle dialysate thromboxane A 2 and prostacyclin concentrations were lower (P<0.05) after training compared with before training. Before training, dialysate thromboxane A 2 decreased with acute exercise, whereas after training, no changes were found. Before training, dialysate prostacyclin levels did not increase with acute exercise, whereas after training there was an 82% (P<0.05) increase from rest to exercise. The exercise-induced increase in ATP and ADP was markedly reduced after training (P<0.05). The amount of eNOS protein in the hypertensive subjects was 40% lower (P<0.05) than in the normotensive control subjects, whereas cystathionine-γ-lyase levels were 25% higher (P<0.05), potentially compensating for the lower eNOS level. We conclude that exercise training alters the balance between vasodilating and vasoconstricting compounds as evidenced by a decrease in the level of thromboxane, reduction in the exercise-induced increase in ATP and a greater exercise-induced increase in prostacyclin.

U2 - 10.1161/HYPERTENSIONAHA.111.176529

DO - 10.1161/HYPERTENSIONAHA.111.176529

M3 - Journal article

C2 - 21896936

SN - 0194-911X

VL - 58

SP - 943

EP - 949

JO - Hypertension

JF - Hypertension

IS - 5

ER -