Parasympathetic Vasodilators 133 



From their experiments Hilton and Lewis eoncluded that the 

 vasodilatation obtained on chorda stimulation, with or without 

 atropine, or after injection of acetylcholine (with no atropine), is 

 due to an intracellular enzyme, in itself without action on the 

 blood vessels. Changes in the gland cells during activity lead to 

 the escape of the enzyme into the interstitial fluid; there the 

 enzyme acts upon protein to form the vasodilator polypeptide. 

 This agent is then removed by the lymph. The enzyme can be 

 detected in the saliva, and the vasodilator activity is, in fact, not 



W ( b ) (c) (d) (e) 



Fig. 7.4. Guinea-pig's ileum suspended in 15 ml. Tyrode solution. 



Effects of 1 ml. perfusate from a submaxillary gland collected during 15 seconds chorda stimu- 

 lation, alone (a) and after 1 minute incubation with 0-2 ml. plasma (b). Effect of 02 ml. plasma (c) 

 and of mixtures of 02 ml. plasma with a freeze-dried concentrate of perfusate (equivalent to 

 4 ml.) collected from a resting gland (d) and from the gland during 1 minute chorda stimulation (e) 

 (Hilton and Lewis, 1955ft). 



to be demonstrated unless the saliva has been in contact with 

 protein to form bradykinin (kallidin). 



Instead of a non-specified metabolite with a vasodilator action, 

 the bradykinin-releasing enzyme, i.e. kallikrein, is considered to 

 be the agent released from the activated gland cells. The "func- 

 tional vasodilatation" of Barcroft seems thereby satisfactorily ex- 

 plained. We are still left with the problem how impulses in the 

 chorda can, after administration of atropine, exert an action on 

 the gland cells which injected acetylcholine cannot: increase the 

 metabolism of the gland and release kallikrein, with a consequent 

 vasodilatation. It may perhaps in addition be asked : is the evidence 



