Brier M E, Bowsher R R, Mayer P R, Henry D P
Department of Medicine, University of Louisville, Kentucky 40292.
Life Sci. 1991;48(9):901-7. doi: 10.1016/0024-3205(91)90037-c.
We used the isolated perfused rat kidney to evaluate the role of renal decarboxylation of p-tyrosine as the source of urinary p-tyramine. Kidneys were perfused with concentrations of p-tyrosine ranging from 0.02 mM to 2.0 mM. p-Tyramine was measured by a sensitive and specific radioenzymatic assay. An increase in the perfusate concentration of p-tyrosine resulted in a significant increase in p-tyramine production that was blocked by the addition of NSD-1015, an inhibitor of aromatic-1-amino decarboxylase (AADC). We conclude p-tyrosine is the precursor for the renal production of p-tyramine, renal AADC catalyzes the formation of urinary p-tyramine, synthesized p-tyramine is predominantly excreted in the urine, and p-tyramine synthesis is modulated by the arterial delivery of p-tyrosine to the kidney.
我们使用离体灌注大鼠肾脏来评估对羟基酪氨酸的肾脏脱羧作用作为尿中对羟基酪胺来源的作用。用浓度范围为0.02 mM至2.0 mM的对羟基酪氨酸灌注肾脏。通过灵敏且特异的放射酶测定法测量对羟基酪胺。对羟基酪氨酸灌注液浓度的增加导致对羟基酪胺生成显著增加，而添加芳香族1-氨基脱羧酶（AADC）抑制剂NSD-1015可阻断这种增加。我们得出结论，对羟基酪氨酸是肾脏生成对羟基酪胺的前体，肾脏AADC催化尿中对羟基酪胺的形成，合成的对羟基酪胺主要经尿液排泄，并且对羟基酪胺的合成受对羟基酪氨酸向肾脏的动脉输送调节。
