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We hypothesized that during its action MPO evokes substantionalvasomotor responses.Methods: Following exposure to MPO (1.92 mU ml-1) in the presence of increasingconcentrations of hydrogen peroxide (H2O2) changes in arteriolar diameter of isolatedgracilis skeletal muscle arterioles (SMAs), and coronary arterioles (CAs) and in theisometric force in basilar arteries (BAs) of the rat were monitored.Results: MPO increased vascular tone to different degrees in CAs, SMAs and BAs.The mechanism of increased vasoconstriction was studied in detail in SMAs. MPO-evoked vasoconstrictions were prevented by the MPO inhibitor 4-aminobenzhydrazide (50 ?M), by endothelium removal in the SMAs. Surprisingly, theHOCl scavenger L-methionine (100 ?M), the thromboxane A2 (TXA2) antagonist SQ-29548 (1 ?M) or the nonspecific cyclooxygenase (COX) antagonist indomethacin (1?M) converted the MPO-evoked vasoconstrictions to pronounced vasodilations inSMAs; not seen in the presence of H2O2. In contrast to norepinephrine-inducedvasoconstrictions, the MPO-evoked vasoconstrictions were not accompanied bysignificant increases in arteriolar [Ca2+ 44 ] levels in SMAs.Conclusion: These data showed, H2O2-derived HOCl to be a potent vasoconstrictorupon MPO application. HOCl activated the COX pathway, causing the synthesis andrelease of TXA2-like substance to increase the Ca2+ 47 sensitivity of the contractileapparatus in vascular smooth muscle cells and thereby to augment H2O2-evokedvasoconstrictions. Nevertheless, inhibition of the HOCl ? 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