Parasympathetic Vasoconstrictors 125 



could be seen to stop completely for a considerable time. A con- 

 tributing factor might be a central inhibition, reducing the flow of 

 parasympathetic secretory impulses. This could, however, not 

 cause a complete cessation of the flow of saliva, since the parotid 

 gland of the sheep secretes spontaneously, even after denervation. 

 The effect was largely abolished by extirpation of the superior 

 cervical ganglion, and since the main effect of sympathetic stimu- 

 lation on the sheep's parotid gland is a vasoconstriction (when the 

 motor fibres have exerted their expelling action) the phenomenon 

 must be interpreted as due chiefly to a sympathetic vasoconstric- 

 tion. Vasoconstriction may thus affect salivary secretion even in a 

 non-anaesthetized animal under fairly physiological conditions. 



PARASYMPATHETIC VASOCONSTRICTORS 



Although the ordinary vascular effect of chorda stimulation is a 

 very striking vasodilatation, some investigators have made obser- 

 vations from which they have inferred that the nerve contains 

 vasoconstrictor fibres. Frohlich and Loewi (1906) found in decere- 

 brate cats that stimulation of the chorda diminished the venous 

 outflow from the submaxillary gland provided that sodium nitrite 

 had been given intravenously or amyl nitrite into the trachea ; this 

 effect was abolished by atropine. Their conclusion was that the 

 nitrites in some way put the dilator fibres of the chorda out of 

 action and that thereby the presence of constrictors can be revealed. 

 Dale (1930) repeated the experiment and saw the same effect of 

 chorda stimulation after nitrites, contrary to Bayliss (1908a); he 

 found it unlikely, however, that the nitrites would have a specific 

 action on the vasodilators, since lowering of the vascular tone by 

 other means, such as hyperventilation or injection of histamine 

 affected the chorda response in the same direction as nitrites. The 

 diminished venous outflow during chorda stimulation under these 

 conditions could, according to Dale, be accounted for by loss of 

 fluid from the blood to the saliva. The observation that the pheno- 

 menon was not found after atropine was, of course, compatible 

 with this explanation also. 



Carlson, Greer and Becht (1907), studying the effect of restricted 

 blood supply on the composition of chorda saliva, had in fact 

 observed that chorda stimulation was followed by a diminished 

 venous outflow when the artery of the submaxillary gland was 

 compressed. This effect was, however, not explained as an action 



