Abstract
Anti-human Ig (immunoglobulin) E induced the release of 2.84 +/- 0.33 ng/ml of immunoreactive leukotrienes (iLTs) from passively sensitized, fragmented rhesus monkey lung, whereas tissue not challenged with anti-IgE released 0.21 +/- 0.08 ng/ml of iLTs spontaneously. Whereas the preferential lipoxygenase inhibitor, nordihydroguaiaretic acid (100 microM), inhibited completely anti-IgE-induced release of iLTs, the calcium channel entry blockers, nifedipine and verapamil (1 and 10 microM), and the purported intracellular calcium antagonist, TMB-8 (100 microM), were without affect on iLT release. The cyclooxygenase inhibitor, indomethacin (5 microM), potentiated iLT release by an average 27.7%. Anti-IgE also induced a contraction of the sensitized monkey lung parenchyma, which was partially suppressed by the antihistamine, mepyramine (10 microM). Against the residual contraction elicited by anti-IgE in the presence of mepyramine, neither FPL 55712 (10 microM) nor verapamil (10 microM) significantly suppressed the contractile activity of anti-IgE. On the monkey lung parenchyma, LTD4 elicited a concentration-dependent contraction, which was antagonized by FPL 55712 (KB = 1 microM) and suppressed by 40 to 50% by verapamil (10 microM). On monkey tracheal rings, the contraction elicited by LTD4 (30 nM) was suppressed by an average 83% by FPL 55712 (10 microM), 47% by verapamil (1 microM) and 45% by TMB-8 (100 microM). In contrast, the KCI-induced contraction was suppressed completely by verapamil and suppressed 79% by TMB-8, suggesting that LTD4 does not elicit contraction of the monkey trachea simply via voltage sensitive calcium entry.(ABSTRACT TRUNCATED AT 250 WORDS)
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