Wakitani K, Cole B R, Geller D M, Currie M G, Adams S P, Fok K F, Needleman P
Am J Physiol. 1985 Jul;249(1 Pt 2):F49-53. doi: 10.1152/ajprenal.1985.249.1.F49.
The effect of atrial peptides on renal function was studied in intact anesthetized dogs. A quantitative comparison of bolus intra-arterial injections demonstrated a rank order potency as renal vasodilators and natriuretic/diuretic agents as follows: ser-leu-arg-arg-atriopeptiin III (SLRR-APIII) greater than high molecular weight artrial peptide greater than or equal to atriopeptin (AP)III = APII much greater than API (essentially inactive). A sustained infusion of APIII was employed in order to study the temporal and quantitative correlation of the renal functional changes induced by the atrial peptide. Both intra-arterial and intravenous administration of the peptide produced concentration-dependent increases in renal blood flow, urine volume, sodium excretion, and osmotic clearance. Infusion of APIII into the renal artery did not alter systemic blood pressure or heart rate. Intravenous infusions of APIII required 10 times higher doses to induce the changes in renal vascular resistance and electrolyte excretion, and a fall in blood pressure and tachycardia resulted. The natriuretic-diuretic effect of the atriopeptins appears to be closely associated with renal vasodilation, exhibiting a positive linear correlation between the peptide-induced changes in sodium excretion and changes in renal blood flow.
在完整的麻醉犬身上研究了心房肽对肾功能的影响。对动脉内推注进行的定量比较显示,作为肾血管扩张剂和利钠/利尿剂,其效力排序如下:丝氨酸 - 亮氨酸 - 精氨酸 - 精氨酸 - 心房肽III(SLRR - APIII)>高分子量心房肽≥心房肽(AP)III = APII>>API(基本无活性)。为了研究心房肽诱导的肾功能变化的时间和定量相关性,采用了持续输注APIII的方法。动脉内和静脉内给予该肽均使肾血流量、尿量、钠排泄和渗透清除率呈浓度依赖性增加。将APIII注入肾动脉不会改变全身血压或心率。静脉输注APIII诱导肾血管阻力和电解质排泄变化所需的剂量高10倍,并且导致血压下降和心动过速。心房肽的利钠 - 利尿作用似乎与肾血管舒张密切相关,在肽诱导的钠排泄变化和肾血流量变化之间呈现正线性相关。