Fine L G, Trizna W
Am J Physiol. 1977 Apr;232(4):F383-90. doi: 10.1152/ajprenal.1977.232.4.F383.
The possibility that prostaglandins (PG) located in the renal medulla may influence renal excretion of sodium by a direct tubular action was examined by the addition of prostaglandins PGE2, PGF2alpha, and PGA2 to the peritubular and luminal surfaces of isolated perfused medullary thick ascending lumbs and collecting tubules from rabbit kidneys. The prostaglandins at both high (2.5 x 10(-4) M) and low (10 (-10) M, 10 (-7) M) concentrations had no effect on transepithelial potential difference and net sodium flux across these segments. Pretreatment of the animals with indomethacin did not influence the results. In vivo, both PGE2 and PGF2alpha, caused a natriuresis when infused directly into one renal artery, whereas PGA2 had no effect on sodium excretion. The prostaglandin inhibitors indomethacin, meclofenamate, and RO 20-5720 similarly had no direct effect on sodium transport in the nephron segments studied. It is concluded that the previously observed influence of prostaglandins and prostaglandin inhibitors on renal excretion of sodium in vivo are not mediated by a direct tubular action.
通过将前列腺素PGE2、PGF2α和PGA2添加到来自兔肾的分离灌流髓质厚升支和集合管的管周和管腔表面,研究了位于肾髓质的前列腺素(PG)是否可能通过直接的肾小管作用影响钠的肾排泄。高浓度(2.5×10⁻⁴M)和低浓度(10⁻¹⁰M、10⁻⁷M)的前列腺素对这些节段的跨上皮电位差和净钠通量均无影响。用吲哚美辛预处理动物不影响结果。在体内,当直接注入一条肾动脉时,PGE2和PGF2α均引起利钠作用,而PGA2对钠排泄无影响。前列腺素抑制剂吲哚美辛、甲氯芬那酸和RO 20-5720同样对所研究的肾单位节段的钠转运无直接影响。得出的结论是,先前观察到的前列腺素和前列腺素抑制剂对体内钠肾排泄的影响不是由直接的肾小管作用介导的。