Damerau B, Roesler J, Vogt W
Br J Pharmacol. 1985 Jan;84(1):55-61.
The slow component of deactivation of guinea-pig isolated ileum to C5adesArg was studied to analyse the mechanism of loss and subsequent recovery of sensitivity. Neither cycloheximide (10(-3) M) nor colchicine (5 X 10(-5) M), vinblastine, lumicolchicine, or cytochalasin B (each 2 X 10(-5) M) affected significantly the spasmogenic effect of C5adesArg or the course of deactivation produced by repeated applications; chloroquine (2 X 10(-4) M) inhibited the spasmogenic effect unspecifically without interfering with deactivation. Recovery from slow deactivation was totally blocked by chloroquine and considerably diminished by colchicine and vinblastine, but was not affected by the other agents. It is proposed that recovery involves lysosomal processing of C5a receptors (occupied by the peptide) but does not require biosynthesis of new receptors.
研究了豚鼠离体回肠对C5adesArg失活的慢成分，以分析敏感性丧失及随后恢复的机制。环己酰亚胺（10⁻³ M）、秋水仙碱（5×10⁻⁵ M）、长春碱、光秋水仙碱或细胞松弛素B（均为2×10⁻⁵ M）均未显著影响C5adesArg的致痉效应或重复给药产生的失活过程；氯喹（2×10⁻⁴ M）非特异性地抑制致痉效应，而不干扰失活过程。氯喹完全阻断了慢失活后的恢复，秋水仙碱和长春碱则显著减弱了恢复，但其他药物未产生影响。研究表明，恢复过程涉及C5a受体（被该肽占据）的溶酶体加工，但不需要新受体的生物合成。
