Takezawa K, Cowley A W, Skelton M, Roman R J
Am J Physiol. 1987 Jun;252(6 Pt 2):F992-1002. doi: 10.1152/ajprenal.1987.252.6.F992.
The effects of atriopeptin III on the renal response to changes in renal perfusion pressure (RPP) were examined in uninephrectomized and adrenalectomized rats. Neural influences on the kidney were eliminated by renal denervation. Plasma levels of antidiuretic hormone (ADH), angiotensin II, aldosterone, corticosterone, and norepinephrine were controlled by intravenous infusion. Infusion of atriopeptin III at a dose of 30 or 100 ng X kg-1 X min-1 increased plasma levels of atrial natriuretic peptide from 101 +/- 8 pg/ml to 424 +/- 16 and 2,553 +/- 308 pg/ml, respectively. In control rats, increasing RPP in two steps from 100 to 125 to 150 mmHg produced sixfold increases in sodium and water excretion. The slopes of the relationships between fractional sodium and water excretion and RPP were enhanced by approximately 10, 20, and 40% in the rats infused with the 30, 100, and 500 ng X kg-1 X min-1 dose of atriopeptin III. Renal blood flow and glomerular filtration rate were not significantly different in vehicle- and atriopeptin III-infused rats at any RPP studied. Papillary blood flow measured with a laser-Doppler flowmeter increased 15% within the first 5 min of infusion of atriopeptin III at a dose of 100 ng X kg-1 X min-1. Cortical blood flow was not significantly altered. The rise in papillary blood flow during atriopeptin III infusion, however, may be a consequence and not the cause of the natriuresis and diuresis, since urine flow increased before significant changes in papillary blood flow were detected. These studies suggest that atrial natriuretic factor could influence the long-term control of arterial pressure by altering renal medullary hemodynamics and promoting the elimination of sodium and water. The plasma levels of atrial natriuretic peptide needed to alter the pressure-natriuresis relationship, however, may exceed levels that can be attained in vivo with endogenous release.
在单侧肾切除和肾上腺切除的大鼠中，研究了心房肽III对肾脏对肾灌注压（RPP）变化反应的影响。通过肾去神经支配消除神经对肾脏的影响。通过静脉输注控制抗利尿激素（ADH）、血管紧张素II、醛固酮、皮质酮和去甲肾上腺素的血浆水平。以30或100 ng·kg⁻¹·min⁻¹的剂量输注心房肽III，可使心房利钠肽的血浆水平分别从101±8 pg/ml升高至424±16和2553±308 pg/ml。在对照大鼠中，将RPP分两步从100 mmHg增加到125 mmHg再增加到150 mmHg，可使钠和水排泄增加6倍。在输注30、100和500 ng·kg⁻¹·min⁻¹剂量心房肽III的大鼠中，钠和水排泄分数与RPP之间关系的斜率分别提高了约10%、20%和40%。在任何研究的RPP下，输注载体和心房肽III的大鼠的肾血流量和肾小球滤过率均无显著差异。用激光多普勒流量计测量的乳头血流量在以100 ng·kg⁻¹·min⁻¹的剂量输注心房肽III的前5分钟内增加了15%。皮质血流量无显著改变。然而，心房肽III输注期间乳头血流量的增加可能是利钠和利尿的结果而非原因，因为在检测到乳头血流量有显著变化之前尿流量就增加了。这些研究表明，心房利钠因子可通过改变肾髓质血流动力学和促进钠和水的排泄来影响动脉压的长期控制。然而，改变压力-利钠关系所需的心房利钠肽血浆水平可能超过内源性释放时体内所能达到的水平。
