Physical training increases eNOS vascular expression and activity and reduces restenosis after balloon angioplasty or arterial stenting in rats.
The effects of dynamic exercise on restenosis after vascular injury are still unknown. The consequences of balloon dilation-induced injury on neointimal hyperplasia, vascular negative remodeling, and reendothelialization were assessed in sedentary and trained rats. Ex vivo eNOS vascular expression and activity were investigated in carotid arteries isolated from sedentary and exercised rats. The in vivo effects of eNOS inhibition by L-NMMA on vessel wall after balloon dilation were evaluated in sedentary and exercised rats. We also investigated the effects of exercise on neointimal formation in a rat stent model of vascular injury. Compared with sedentary group, the arteries isolated from trained rats showed higher levels of eNOS protein expression and activity 7 days after balloon dilation. A significant reduction of both neointimal hyperplasia and negative remodeling was observed 14 days after balloon injury in trained compared with sedentary rats. Moreover, we demonstrated that exercise training produced accelerated reendothelialization of the balloon injured arterial segments compared with sedentary. L-NMMA administration eliminated the benefits of physical training on vessel wall after balloon dilation. Finally, a decrease of neointimal hyperplasia as well as of platelet aggregation was observed after stent deployment in trained rats compared with sedentary. In conclusion, physical exercise could favorably affect restenosis after balloon angioplasty and stenting. Increase in eNOS expression and activity might contribute to the potential beneficial effects of exercise on the vessel wall after vascular injury.
Indolfi
Ciro
C
Division of Cardiology, Magna Graecia University, Catanzaro, Italy. indolfi@unicz.it
Torella
Daniele
D
Coppola
Carmela
C
Curcio
Antonio
A
Rodriguez
Francisca
F
Bilancio
Antonio
A
Leccia
Antonio
A
Arcucci
Oreste
O
Falco
Mariacristina
M
Leosco
Dario
D
Chiariello
Massimo
M
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000800:Angioplasty, Balloon / Q000009:adverse effects*; D000818:Animals; D016893:Carotid Stenosis / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D002455:Cell Division / Q000502:physiology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000201:enzymology / Q000293:injuries / Q000473:pathology; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006083:Graft Occlusion, Vascular / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D006965:Hyperplasia / Q000473:pathology / Q000517:prevention & control; D015151:Immunoblotting; D007150:Immunohistochemistry; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D010805:Physical Conditioning, Animal; D005082:Physical Exertion; D010974:Platelet Aggregation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015607:Stents / Q000009:adverse effects; D013550:Swimming / Q000502:physiology; D017539:Tunica Intima / Q000187:drug effects / Q000201:enzymology / Q000293:injuries / Q000473:pathology; D019323:omega-N-Methylarginine / Q000494:pharmacology
D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D000244:Adenosine Diphosphate; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat