Evidence for Uneven Alpha-Receptor Distribution in the Rat Portal Vein
The smooth muscle of the rat portal vein which supports propagation becomes supersensitive to exogenous l-norepinephrine after elimination of the vessel's intramural neuronal uptake mechanism. Such supersensitivity is generally associated with intimate neuromuscular connections. Since the adrenergic vasomotor fibers in the portal vein do not enter the muscle tissue, it has been proposed that muscle cells close to the nerve terminals must determine the response to norepinephrine. With the aim of elucidating the mechanism behind the prejunctional supersensitivity, the total uptake of labeled norepinephrine in the portal vein was analyzed and its distribution within the vessel wall was evaluated directly using isotopically labeled frozen sections. The total uptake of the portal vein, related to its endogenous norepinephrine content, was comparable with that in other vascular and nonvascular tissues. The 3H-uptake profile of the vessel wall showed that the neurogenic uptake was confined to the narrow adrenergic plexus between the longitudinal and the circular muscle layers. The neuronal uptake mechanism therefore could only influence the concentration of exogenous norepinephrine at muscle cells close to the nerve terminals. These results support the hypothesis that the prejunctional supersenstivity in the rat portal vein indicates that the alpha receptors are located on muscle cells in the vicinity of the adrenergic nerve terminals.
- 3H-l-norepinephrine uptake
- prejunctional supersensitivity
- Received July 24, 1972.
- Accepted March 7, 1973.
- © 1973 American Heart Association, Inc.