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.
Sotníková
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Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava, Slovakia.
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D019335:Nitroarginine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; D019335:Nitroarginine; D006861:Hydrogen Peroxide; D002118:Calcium