Evidence that vasoactive intestinal polypeptide is a dilator transmitter to some cerebral and extracerebral cranial arteries.
Many arteries of the head upon electrical stimulation of the non-adrenergic nerve terminals present in their wall exhibit dilation that is only partially reduced by atropine. The results of three types of experiments are presented that tend to implicate vasoactive intestinal polypeptide (VIP) a known vasodilator, as an atropine-resistant dilator transmitter. VIP activity is high in vessels that exhibit neurogenic dilation and low in those that do not. It is released from two arteries that show such dilation upon neurogenic field stimulation and VIP antiserum reduces neurogenic dilation. It is proposed that VIP as well as acetylcholine are released from the innervation of some cranial arteries and together in a number of animals of least are responsible for part of the complex neurogenic dilation witnessed in these vessels. Although substance P is present in nerves found within the wall of cerebral and other cranial blood vessels, it is either ineffective as a dilator in vessels that show a sizeable dilation to electrical stimulation, or else exhibits marked, rapid, persistent tachyphylaxis.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000906:Antibodies; D000936:Antigen-Antibody Complex; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D002415:Cats; D002536:Cerebral Arteries / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005260:Female; D008297:Male; D014660:Vasoactive Intestinal Peptide / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents
D000906:Antibodies; D000936:Antigen-Antibody Complex; D014665:Vasodilator Agents; D014660:Vasoactive Intestinal Peptide; D000109:Acetylcholine