[3H]noradrenaline [( 3H]NA) uptake studies were carried out in cat hypogastric nerves ligated in vivo, 2 cm distal to the inferior mesenteric ganglion, for different time periods. Atria from the same animals served as controls to determine the uptake of the amine by the U1 uptake system present in noradrenergic nerve terminals. The net uptake of [3H]NA by hypogastric nerves increased with time of ligation, reaching a maximum 24 h after ligation in the segment of nerve immediately proximal to the ligature (P1 segment, neurosome). No further increase in uptake was observed at 48 or 72 h. Segments distal (D1) to the ligature also retained significant amounts of [3H]NA. In both cases the uptake was blocked by cocaine (3 microM). Reserpine pre-treatment (2 mg/kg I.M.) markedly decreased the endogenous NA content to 1-2% of untreated cats and the net uptake of [3H]NA was lowered to 25% both in cat hypogastric nerve and atria. The uptake was further decreased in the presence of cocaine (3 microM). 6-Hydroxydopamine (100 microM) did not modify the [3H]NA uptake by ligated cat hypogastric nerves but almost abolished the [3H]NA net uptake by right atria from the same animals. After collagenase pre-treatment (0.05% for 15 min) the net uptake of [3H]NA was not altered in the atrium. However, collagenase-pre-treated ligated nerves, took up almost twice as much [3H]NA; under these conditions, 6-hydroxydopamine produced a marked decrease in [3H]NA net uptake. These data suggest the presence in the perineurium of a diffusion barrier for very polar substances, including 6-hydroxydopamine. In conclusion, our data demonstrate that the cat hypogastric nerve ligated in vivo has a cocaine-sensitive system for NA uptake which resembles the NA uptake mechanism (U1) present in noradrenergic nerve terminals. Our data further support the view that the ligated cat hypogastric nerve (neurosome) could be considered as a model of noradrenergic nerve terminal free of effector cell.
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