Damerau B, Roesler J, Vogt W
Br J Pharmacol. 1985 Jan;84(1):63-9.
The fast component of deactivation of guinea-pig isolated ileum to the spasmogenic action of the complement peptide C5adesArg was further differentiated from the slow component which had been previously analysed (Damerau et al., 1985a, b). Fast deactivation differs from the slow component in the following characteristics: (a) it is unspecific in that it is also induced by C3a, another complement peptide, (b) it depends on the spasmogenic effect of the peptides, and (c) it does not occur at 16 degrees C. In contrast to the slow component, in which the deactivation is thought to be caused by blockade of C5a receptors, fast deactivation seems to be due to a transient increase of intracellular cyclic AMP evoked by C5adesArg and C3a; it is prevented by GDP beta S (5 X 10(-4) M) which blocks activation of adenylate cyclase, and prolonged by agents which sustain cyclic AMP elevations, namely 5 X 10(-4) M theophylline and 5 X 10(-4) M) GTP gamma S.
豚鼠离体回肠对补体肽C5adesArg致痉作用失活的快速成分，进一步与先前分析过的缓慢成分区分开来（达梅劳等人，1985年a、b）。快速失活与缓慢成分在以下特征方面有所不同：（a）它是非特异性的，因为它也可由另一种补体肽C3a诱导；（b）它取决于肽的致痉作用；（c）在16℃时不发生。与缓慢成分不同，缓慢成分的失活被认为是由C5a受体的阻断引起的，快速失活似乎是由于C5adesArg和C3a引起的细胞内环状AMP的短暂增加；它可被阻断腺苷酸环化酶激活的GDPβS（5×10⁻⁴M）阻止，并被维持环状AMP升高的试剂延长，即5×10⁻⁴M的茶碱和5×10⁻⁴M的GTPγS。
