Miscellaneous Agents 87 



nounced excitation of the central nervous system. They have 

 muscarine-like actions, demonstrated on the blood pressure and 

 the pupil, and nicotine actions on sympathetic ganglia as shown on 

 the nictitating membrane and, after atropine, on the blood pres- 

 sure. In vitro experiments show that they can inhibit acetylcholine 

 esterase. 



Esterase inhibition, however, cannot be the cause of the saliva- 

 tion, for a normal activity of the enzyme was found in a gland that 

 had responded to HN2. Central or sympathetic ganglionic effects 

 cannot be the main causes, since the flow is obtained after acute 

 section of the chorda and removal of the superior cervical ganglion. 

 A muscarinic action seems to be mainly responsible for the sali- 

 vation. In the strange two-phase response and in the lack of 

 atropine antagonism in the second phase (if the atropine is not 

 given early) nitrogen mustard differs from the ordinary muscarine- 

 like drugs. Hunt and Philips assume that even the second phase of 

 secretion is due to a reaction between the drug and "cholinergic 

 receptors"; this reaction, when it has once taken place, is not 

 antagonized by atropine. Alternatively, it has been suggested that 

 the agent excites the gland cells "directly" (Gaddum and Foss). 

 Obviously, the mechanism of action is obscure and warrants further 

 study (Hunt and Philips, 1949). 



Secretagogne substances in saliva. According to Demoor (19 13) 

 saliva contains agents which are able to stimulate secretion from 

 the salivary glands. Guimarais (1932, 1936a and b, 1938) and 

 Guimarais and Tavares (1942a and b) have further studied the 

 secretory activity of saliva. When saliva is injected into the artery 

 of the submaxillary gland an abundant secretion is evoked. The 

 agent causing this effect is not identical with that which on intra- 

 venous injection lowers the blood pressure, i.e., kallikrein. It has 

 been suggested that the chemical transmitters of the secretory 

 nerves or injected secretory drugs, cause the release of the secre- 

 tory agent from an inactive state ; the agent then acts on the gland 

 cells to cause a flow of saliva. When considering this agent as a 

 general, ultimate mediator for salivary secretion it must be kept in 

 mind that its secretory effects are abolished by atropine. Further 

 experiments seem required to throw light on the possible physio- 

 logical role of this interesting agent. 



