Functional evidence that balloon angioplasty results in transient nitric oxide synthase induction.

Since serious vasospastic episodes limit the efficacy of percutaneous transluminal coronary angioplasty, this study has examined the time-dependent changes in vascular reactivity that occur following rat carotid artery balloon angioplasty. Relative to vessels from sham-operated animals, angioplasty caused an immediate increase in endothelin-1 contractile potency, an observation not made with noradrenaline or KCl, implicating endothelin-1 in the pathogenesis of acute arterial vasospasm. This hyperreactivity, possibly resulting from the loss of endothelin-1-induced nitric oxide release from the endothelium, was transient and was followed by a non-specific decrease in reactivity to all three spasmogens. Since the delayed reduction in endothelin-1 contractile potency was restored by N omega-nitro-L-arginine methyl ester, this hyporeactivity appeared to result from nitric oxide synthase induction. Furthermore, since the regenerating endothelium was dysfunctional, the generation of nitric oxide was from a non-endothelial source (possibly the smooth muscle or infiltrating macrophages). This response may function to ameliorate the spasmogenic and proliferative actions of chronically acting vasoactive factors and oppose platelet aggregation.