Structural and functional ontogenetic development of the rat portal vein after neonatal 6‐hydroxydopamine treatment

The importance of the adrenergic vasomotor nerve supply for the vascular ontogenetic development has been studied in the isolated portal vein preparation from rats, at 5–6 weeks of age, who had either been chemically sympathectomized by a series of postnatal 6‐hydroxydopamine (6‐OHDA) injections or been receiving the solvent alone. It was found that 6‐OHDA treatment largely, but not completely, prevented the outgrowth of the terminal NA fluorescent ground plexus. Nevertheless, the media underwent a seemingly normal differentiation into two layers. Functionally, the portal vein from the 6‐OHDA treated animals displayed weak and non‐persistent myogenic spontaneous activity; sensitivity to exogenous noradrenaline (NA) was increased 3‐fold and maximum stress was increased by 25 % as compared to control. Responses to transmural field stimulation were only obtained at high impulse rates and the maximum response was attenuated. Considering the very sparse adrenergic innervation following 6‐OHDA they seemed surprisingly large, however, but since they were abolished by tetrodotoxin and by phenoxybenzamine responses are concluded to be neurogenic and adrenergic in origin. A singular attenuation of neurogenic responses by atropine was found in 6‐OHDA treated vessels but not in controls. It is concluded that the adrenergic vasomotor nerve supply seems to exert some trophic influence during ontogenetic development but that the morphologic vascular development is largely governed by other, non‐neurogenic mechanisms. As to functional development, 6‐OHDA induced sympathectomy causes impaired development of phasic myogenic activity whereas maximum stress is augmented as is the tissue sensitivity to exogenous NA.