Nushiro N, Abe K, Seino M, Yoshinaga K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Am J Physiol. 1988 Apr;254(4 Pt 2):F521-6. doi: 10.1152/ajprenal.1988.254.4.F521.
To examine whether amiloride, an inhibitor of a conductive sodium channel in the distal tubule, modifies a possible tubular action of atrial natriuretic peptide (ANP), alpha-human ANP (0.05 micrograms.kg-1.min-1) was infused intravenously with or without pretreatment of amiloride (5 mg/kg + 0.04 mg.kg-1.min-1) in anesthetized rabbits. No significant changes in arterial pressure and renal blood flow were observed between two groups after ANP infusion. However, increases in filtered sodium load (FNa) and net tubular sodium reabsorption (RNa) induced by ANP were attenuated after the amiloride pretreatment. These attenuations in FNa and RNa could be due to the failure of increase in glomerular filtration rate, although the reason is not clear. Amiloride pretreatment abolished the ANP-induced kaliuresis, whereas ANP-induced increases in urinary sodium and fractional sodium excretion were additive after amiloride pretreatment. Thus, ANP elicited a further natriuretic effect even when the amiloride-sensitive component was blocked. This suggests that there is another mechanism by which ANP induces natriuresis, in addition to any ANP effects mediated by interference with sodium conductive channels.
为了研究远端小管中钠传导通道抑制剂氨氯地平是否会改变心房利钠肽(ANP)可能的肾小管作用,在麻醉兔中静脉输注α-人ANP(0.05微克·千克⁻¹·分钟⁻¹),同时进行或不进行氨氯地平预处理(5毫克/千克 + 0.04毫克·千克⁻¹·分钟⁻¹)。输注ANP后,两组之间的动脉血压和肾血流量均未观察到显著变化。然而,氨氯地平预处理后,ANP诱导的滤过钠负荷(FNa)增加和肾小管钠净重吸收(RNa)增加减弱。FNa和RNa的这些减弱可能是由于肾小球滤过率未能增加,尽管原因尚不清楚。氨氯地平预处理消除了ANP诱导的尿钾增多,而氨氯地平预处理后,ANP诱导的尿钠和钠排泄分数增加是相加的。因此,即使氨氯地平敏感成分被阻断,ANP仍能引发进一步的利钠作用。这表明,除了通过干扰钠传导通道介导的任何ANP效应外,ANP诱导利钠还有另一种机制。