Donowitz M, Cusolito S, Battisti L, Fogel R, Sharp G W
J Clin Invest. 1982 Apr;69(4):1008-16. doi: 10.1172/jci110504.
The effects of dopamine on active intestinal ion transport have been evaluated. An epithelial sheet preparation of rabbit ileum was used in vitro with the Ussing chamber-voltage clamp technique. Dopamine, in the presence of 1 mM ascorbic acid, added to the serosal bathing solution caused a dose-dependent decrease in short-circuit current, with a half-maximal effect at 1.2 muM and maximal effect of -50 muA/cm(2) at 50 muM; dopamine decreased the potential difference, and increased the conductance and net Na and net Cl absorption. There was no effect on the residual ion flux. Dopamine did not alter the change in short-circuit current caused by mucosal glucose (10 mM) or serosal theophylline (10 mM). Mucosal dopamine had no effect. The effect of dopamine on short-circuit current was inhibited by the dopamine antagonists haloperidol and domperidone and the alpha(2)-adrenergic antagonist yohimbine; there was no effect of the alpha(1)-antagonist prazosin and the beta-antagonist propranolol. In addition, the alpha(2)-adrenergic agonist clonidine, but not the alpha(1)-agonist methoxamine caused a dose-dependent decrease in short-circuit current. The ileal effects of dopamine did not occur via conversion into norepinephrine or release of norepinephrine from the peripheral nerves since "peripheral sympathectomy" with 6-hydroxydopamine did not alter the dopamine-induced change in ileal short-circuit current. The dopamine effects were not associated with a change in basal ileal cyclic AMP content but were associated with a decrease in total ileal calcium content as measured by atomic absorption spectrometry and as estimated by (45)Ca(++) uptake. The decrease in calcium content could be attributed to a dopamine-induced decrease in (45)Ca(++) influx from the serosal surface. Because of the presence of dopamine in ileal mucosa and these effects on ileal electrolyte transport, it is possible that dopamine may be involved in the physiologic regulation of active intestinal electrolyte absorption.
已评估了多巴胺对活跃肠离子转运的影响。采用乌斯电极槽 - 电压钳技术，在体外使用兔回肠的上皮片制备物。在存在1 mM抗坏血酸的情况下，将多巴胺添加到浆膜侧浴液中会导致短路电流呈剂量依赖性降低，在1.2 μM时达到半数最大效应，在50 μM时最大效应为 -50 μA/cm²；多巴胺降低了电位差，增加了电导以及净钠和净氯吸收。对残余离子通量没有影响。多巴胺不会改变由黏膜葡萄糖（10 mM）或浆膜茶碱（10 mM）引起的短路电流变化。黏膜侧多巴胺没有作用。多巴胺对短路电流的作用被多巴胺拮抗剂氟哌啶醇和多潘立酮以及α₂ - 肾上腺素能拮抗剂育亨宾抑制；α₁ - 拮抗剂哌唑嗪和β - 拮抗剂普萘洛尔没有作用。此外，α₂ - 肾上腺素能激动剂可乐定，但不是α₁ - 激动剂甲氧明，会导致短路电流呈剂量依赖性降低。多巴胺对回肠的作用不是通过转化为去甲肾上腺素或从外周神经释放去甲肾上腺素而发生的，因为用6 - 羟基多巴胺进行“外周交感神经切除术”并没有改变多巴胺诱导的回肠短路电流变化。多巴胺的作用与基础回肠环磷酸腺苷含量的变化无关，但与通过原子吸收光谱法测量以及通过⁴⁵Ca²⁺摄取估计的回肠总钙含量的降低有关。钙含量的降低可归因于多巴胺诱导的⁴⁵Ca²⁺从浆膜表面流入的减少。由于回肠黏膜中存在多巴胺以及这些对回肠电解质转运的影响，多巴胺可能参与了活跃肠电解质吸收的生理调节。
