Substantial evidence of postangioplasty vasoconstriction is available, both at the dilated site and distal to balloon injury, demonstrating its frequent occurrence. It is likely that even mild or moderate vasoconstriction at the site of balloon injury may create flow turbulence, promoting platelet aggregation and contributing to thrombotic vessel closure. The regulation of arterial smooth muscle tone is a complex process and should be distinguished from elastic recoil, which occurs at the site of balloon injury due to passive elastic properties of the artery, generally immediately after balloon deflation. The contribution of a variety of messengers generated by humoral, neurogenic, myogenic, and endothelium-derived factors in this regulatory process has been implicated. The possible mechanisms of post-percutaneous transluminal coronary angioplasty vasoconstriction at the dilated site (local) and in segments of coronary artery beyond the dilated site (distal) are reviewed in this article.