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1. The object of the present experiments was to re-investigate the role of kallikrein in functional hyperaemia in the submaxillary gland of the cat. Kallikrein concentration in the gland and saliva was reduced by ligation of the duct for 2-3 days before the acute experiment, at which time the duct was cannulated proximal to the ligation and blood flow and salivation measured.

2. Despite the fall in kallikrein concentration, a normal two-phase vascular response was obtained on continuous stimulation of the chorda-lingual nerve at 1-5 Hz and the progressive increase in blood flow to a constant level characteristic of 10 and 20 Hz stimulation was also seen. Quantitatively, the increase in blood flow following a 10 sec stimulation was reduced to about 75% of control values at all stimulation frequencies used and the maintained vasodilatation was reduced when using continuous stimulation at 1 Hz but not at 10 and 20 Hz.

3. The supersensitivity to the vasodilator properties of bradykinin, previously reported to follow duct ligation, was confirmed.

4. The increased blood flow produced by chorda-lingual nerve stimulation could be delayed by circulatory arrest. Evidence was obtained suggesting that the vascular response to chorda stimulation delayed by arterial occlusion was not mediated by kallikrein alone.

5. It was concluded that kallikrein was not the sole mediator of functional hyperaemia in the cat submaxillary gland but that a combination of vasodilator nerves and kallikrein release explained more phenomena than either hypothesis alone.