Investigation of the mechanisms underlying H2O2-evoked contraction in the isolated rat aorta.
1. H2O2 (20-200 microM) elicited concentration-dependent contraction of rat isolated aortic rings. Pretreatment of the preparations with N-nitro-L-arginine (L-NNA) or removal of the endothelium augmented significantly the contractile response of rings to H2O2. The increase of the extracellular potassium concentration ([K+]o) resulted in a K(+)-dependent increase of the contractile response. 2. In Ca(2+)-free physiological salt solution (PSS), responses to H2O2 were decreased approximately to 4% of the 100 mM KCl-induced response. 3. In addition, calcium channel blockers (nisoldipine, nifedipine, verapamil, flunarizine) did not completely inhibit H2O2-induced contractions. 4. H2O2-evoked contractions were abolished after repeated applications of caffeine or noradrenaline in Ca(2+)-free PSS. 5. Both extracellular Ca2+ entry through voltage-dependent Ca2+ channels and intracellular Ca2+ from caffeine- and noradrenaline-sensitive stores appear to participate in H2O2-induced contractions of rat aortic rings.