Secretion of kallikrein and its role in vasodilatation in the submaxillary gland

1. The effects of parasympathetic (chorda) and sympathetic nerve stimulation on the concentration and output of kallikrein secreted in saliva from the cat's submaxillary gland were compared. Sympathetic stimulation always produced a much higher concentration (up to 500 times) and output (up to 390 times) of kallikrein than parasympathetic stimulation. In the dog, in which sympathetic nerve stimulation produces little or no secretion from the submaxillary gland, there was also a marked increase in the secretion of kallikrein when sympathetic was superimposed on parasympathetic secretion. This effect did not occur, however, in the rabbit's submaxillary gland. 2. It was possible to deplete the cat's submaxillary gland of kallikrein, either by ligation of the duct for several days or by duct ligation and sympathetic nerve stimulation, so that it was undetectable either in the gland or in saliva after stimulation of the chorda. Such glands, nevertheless, responded to chorda stimulation with a normal atropine‐resistant vasodilatation. 3. There is a close parallelism between the rate of secretion of salvia and vasodilatation over a range of frequencies of chorda stimulation, but the output (and concentration) of kallikrein in saliva is distinctly different for the same frequencies of nerve stimulation. 4. Our results are consistent with the view that vasodilator nerves exist in the parasympathetic nerves to the submaxillary gland. We suggest that they are cholinergic in nature despite the fact that chorda vasodilatation is resistant to atropine. It is further suggested that neither the kallikrein—kinin system nor adrenergic vasodilator nerve fibres play a significant role in chorda vasodilatation.