Abstract
Summary
Mouse saliva contains a potent inhibitor of complement activity. The secretion of this inhibitor appears to be regulated by action on α-adrenergic receptors for two reasons. First, an α-agonist (norepineph-rine) elicited saliva with a 260-fold higher specific activity of the inhibitor than that obtained with a cholinergic agent (pilocar-pine). Second, the α-agonist elicited saliva having a 43-fold greater specific activity than that obtained following administration of a β-adrenergic agonist (isoproterenol). This anticomplementary factor probably proteolytically degrades one or more of the complement components since it is inhibited by several protease inhibitors. The salivary anticomplementary factor is more potent than trypsin, chymotrypsin, thrombin, or Kallikrein. The anticomplementary factor has a pattern of inhibition like that of Kallikrein but unlike those of trypsin or chymotrypsin.
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