FURTHER EVIDENCE FOR A MUSCARINIC COMPONENT TO THE NEURAL VASODILATOR INNERVATION OF CEREBRAL AND CRANIAL EXTRA-CEREBRAL ARTERIES OF THE CAT

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 2 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 significantly potentiates 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. Apparently, there are 2 transmitters released in parallel from nerve(s) in the walls of cerebral, lingual and, possibly, other cranial arteris to cause vasodilation. It seems likely that one of these is acetylcholine.