Guthrie S D, Murphy Q R
Proc Soc Exp Biol Med. 1976 Jan;151(1):117-20. doi: 10.3181/00379727-151-39156.
The effects of catecholamines on hepatic K+ and Na+ movements were studied in anesthetized dogs by measuring systemic arterial and hepatic venous electrolyte composition following intraportal injections of adrenergic agonists. All catecholamines studied caused the initial loss and subsequent uptake of K+ by the liver. The loss of hepatic K+ was accompanied by an uptake of Na+ at a 1:1 ratio. This accumulation of Na+ continued, although at a slower rate, for at least 8 min. Epinephrine and norepinephrine were much more potent in these effects than either phenylephrine or isoproterenol. Neither alpha- nor beta-adrenergic blockade, singly or in combination, had an appreciable effect on the magnitude or duration of the observed ion shifts. It is concluded that the predominant effect of catecholamines is to produce a net accumulation of hepatic Na+, and that the mechanism governing hepatic ion movements is nonadrenergic as defined by stimulation by specific adrenergic agonists and inhibition by specific adrenergic antagonists.
通过在门静脉内注射肾上腺素能激动剂后测量全身动脉和肝静脉电解质组成，研究了儿茶酚胺对麻醉犬肝脏钾离子和钠离子转运的影响。所研究的所有儿茶酚胺均导致肝脏最初丢失钾离子，随后又摄取钾离子。肝脏钾离子的丢失伴随着钠离子以1:1的比例摄取。钠离子的这种蓄积至少持续8分钟，尽管速率较慢。在这些作用中，肾上腺素和去甲肾上腺素比苯肾上腺素或异丙肾上腺素的作用要强得多。单独或联合使用α-或β-肾上腺素能阻滞剂对观察到的离子转移的幅度或持续时间均无明显影响。得出的结论是，儿茶酚胺的主要作用是使肝脏钠离子净蓄积，并且控制肝脏离子转运的机制是非肾上腺素能的，这是由特定肾上腺素能激动剂的刺激和特定肾上腺素能拮抗剂的抑制所定义的。
