Parasympathetic Vasodilators 131 



motor contracture" in the tongue after previous section of the 

 hypoglossal nerve. In order to elicit the contracture they stimulated 

 the intramedullary portion of the seventh nerve and the reticular 

 matter close to it, using a concentric bipolar electrode. Contrac- 

 tures were always accompanied by marked salivation ; the glandular 

 blood flow was not measured, but that of the tongue was recorded 

 and found to increase at the same time. Judging from these experi- 

 ments it seems unlikely that it would be possible to separate 

 secretory and vascular effect by intramedullary stimulation. 



A remarkable contribution to the discussion concerning the 

 vasodilatation in the submaxillary gland was made by Ungar and 

 Parrot (1936) in a paper, which apparently did not attract much 

 attention at the time of its publication. These authors studied the 

 vasodilator activity of saliva, then recently discovered and inves- 

 tigated by several research workers (Bellis and Scott, 1933; 

 Seeker, 1934; Feldberg and Guimarais, 1935; Gibbs, 1935; Lar- 

 son, 1935). Ungar and Parrot found the activity to be due to kal- 

 likrein, described by Frey and Kraut (1928). Werle and Roden 

 (1936) came to the same conclusion. The French investigators 

 launched the hypothesis that kallikrein "jouait le role d'interme- 

 diaire chimique dans la vasodilatation locale" during stimulation 

 of the chorda. 



Our knowledge of the vasodilatation in the submaxillary gland 

 has been greatly widened by a series of investigations by Hilton 

 and Lewis (1955a and b, 1956). They found that the injection of 

 botulinum toxin into the gland abolished simultaneously the secre- 

 tory and vasodilator responses to chorda stimulation. Since this 

 agent is assumed to paralyse preferentially cholinergic fibres they 

 concluded that non-cholinergic fibres are not concerned in the 

 vasodilatation. So far, their opinion is in agreement with that of 

 Dale and Gaddum. Further experiments, however, led them to the 

 conclusion that the agent causing the vasodilatation is not acetyl- 

 choline, set free from dilator fibres, but some more stable agent, 

 produced or released in connection with the activity in the gland, 

 even in the presence of atropine. Fig. 7.3 shows one of their 

 experiments. It is apparent from this figure that the vasodilatation 

 on stimulation of the chorda can be delayed by arterial occlusion ; 

 the same is true for the dilatation produced by injected acetyl- 

 choline. Venous occlusion, on the other hand, delays the dilator 

 response only when the lymph drainage has been blocked. From 



