Sympathetic Innervation of Cerebral Arteries: Prejunctional Supersensitivity to Norepinephrine After Sympathectomy or Cocaine Treatment

The inactivation of the norepinephrine transmitter in the region of the adrenergic receptor is one important function of the sympathetic nerve terminals innervating blood vessels. This capacity was tested on isolated cat's middle cerebral artery (MCA) by recordings of the contractile response induced by norepinephrine at various stages after sympathectomy (excision of the superior cervical ganglion). Within three days after denervation, when fluorescence microscopy revealed a disappearance of neuronal norepinephrine in the vessel wall, there was a threefold increase in sensitivity of the test system which was not further enhanced at two weeks. This, and the finding of a similar amount of sensitization (of non-denervated vessels) to norepinephrine or tyramine after cocaine treatment, showed that a prejunctional type of sensitivity had developed. The sympathetic denervation did not influence the dose-response curve obtained with acetylcholine, supporting the specific nature of the supersensitivity reaction only to the sympathetic transmitter. Half a year after sympathectomy the sensitivity of the pial arteries to norepinephrine returned to control levels despite the absence of reinnervation, indicating that postjunctional changes also occurred. The findings offer further evidence for a functional role of the sympathetic nerves supplying intracranial arteries and show that the mode of innervation resembles that found in peripheral vessels.