136 Blood Flow and Secretion 



which sympathetic stimulation did not cause any secretion, vaso- 

 constriction was the only vasomotor effect obtained. Priscol, on 

 the other hand, reduces the sympathetic constriction, leaving the 

 secretion ; the vasodilatation is, likewise, retained. When this drug 

 has been given vasoconstriction does not interfere with the dilata- 

 tion, which is then obtained early in the stimulation period; the 

 ordinary, characteristic vasodilatation when the sympathetic stimu- 

 lation is discontinued, and which is sometimes as pronounced as 

 during chorda stimulation, is not obtained after priscol. 



All these observations are compatible with the view that the 

 sympathetic dilatation is secondary to the secretion and due to 

 some vasodilator agent appearing during glandular activity. The 

 constrictor response obtained shortly after the start of a stimula- 

 tion period favours the accumulation of the agent and the constric- 

 tion diminishes ; there may even temporarily be a period of marked 

 dilatation. If so, the dilator agent is quickly removed and constric- 

 tion again gets the upper hand. In this way, periods of constriction 

 and dilatation may sometimes alternate. On cessation of stimula- 

 tion the dilator agent, unopposed by constrictor impulses, causes 

 a marked dilatation. After priscol, however, the constrictor fibres 

 are without effect and the agent is able to guarantee an adequate 

 blood supply during the stimulation period already, and there is 

 no marked reactive hyperaemia afterwards. 



Experiments by Hilton and Lewis (1956) suggest that the func- 

 tional dilatation during sympathetic stimulation is due to the for- 

 mation of a bradykinin-like agent. 



In some cats there is evidence suggesting the presence of vaso- 

 dilator fibres for the submaxillary gland in the sympathetic trunk 

 (Emmelin, 19550). The dilatation was in these instances obtained 

 very early in the stimulation period and came to light when both 

 secretion and constriction had been abolished by a sympathicolytic 

 agent. This effect was not abolished by atropine. 



REFERENCES 



anrep, G. v. and R. K. cannan (1922). The metabolism of the salivary 

 glands. III. The blood sugar metabolism of the submaxillary gland. 

 J. Physiol, 57, 1-6. 



anrep, g. v. and c. L. evans (1920). The mode of action of vaso-dilator 

 nerves, jf. Physiol., 54, x-xi. 



