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Transmural electrical stimulation of segments of lingual and cerebral (basilar, middle and posterior cerebral) and also other cranial arteries of the cat results after a long latency in a dilator response. The response may be resolved into two components--an initial transient atropine-sensitive component and a slower more ponderous one that is atropine-resistant. The variability in pattern of dilation responses from segments of different vessels or even those from the same segment of different cats is considerable. Some responses are entirely atropine-sensitive and others atropine-resistant; however the vast majority show a dilation that can be considered to be made up of both components. The latencies of the atropine-sensitive and atropine-resistant components are not different. The effect of atropine on the lingual but not the cerebral arteries is frequency dependent, being proportionately greater at low than at high frequencies. In both vessels, the effect of atropine is independent of train length at 1 Hz. Physostigmine potentiates significantly the dilation of the lingual artery but not that of the cerebral arteries. The potentiation is reversed by atropine. The endogenous acetylcholine level was measured in a series of vessels. It can be correlated with the activity of choline acetyltransferase and the presence of neurogenic dilation. It is proposed that there are two transmitters released in parallel from nerve(s) in the walls of cerebral, lingual, and possibly, other cranial arteries to cause vasodilation. It seems that one of these is acetylcholine.

Further evidence for a muscarinic component to the neural vasodilator innervation of cerebral and cranial extracerebral arteries of the cat.