Keeler R, Azzarolo A M
Can J Physiol Pharmacol. 1983 Sep;61(9):996-1002. doi: 10.1139/y83-149.
The intravenous injection of an extract of atrial myocardium into anesthetized rats during a hypotonic diuresis resulted in an increase in the renal excretion of water, sodium, potassium, calcium, magnesium, and phosphate. There was an increase in urine concentration which was probably a result of the secretion of vasopressin since it did not occur in Brattleboro (di/di) rats. A transient increase in glomerular filtration rate and renal plasma flow occurred during the first five minutes with a more sustained rise in filtration fraction. Injection of atrial extract also caused a partial inhibition of solute-free water formation in Brattleboro rats subjected to water diuresis and a partial inhibition of solute-free water reabsorption in rats subjected to maximal antidiuresis by infusing vasopressin. In neither case was the degree of inhibition as profound as that observed after injecting furosemide in a dose which caused a comparable natriuretic response. A large dose of furosemide blocked the natriuretic response to atrial extracts whereas, when a comparable level of sodium and water output was produced by massive infusions of saline, the natriuretic response to atrial extract was increased. It is suggested that atrial natriuretic factor might inhibit sodium transport in nephron segments beyond the medullary thick ascending limb. Furosemide might also act at the same tubular site or inhibit tubular secretion of the atrial natriuretic factor.
在低渗性利尿期间,将心房肌提取物静脉注射到麻醉大鼠体内,会导致水、钠、钾、钙、镁和磷酸盐的肾排泄增加。尿浓缩增加,这可能是抗利尿激素分泌的结果,因为在布拉特洛维(di/di)大鼠中未出现这种情况。在最初五分钟内,肾小球滤过率和肾血浆流量短暂增加,滤过分数持续升高。注射心房提取物还会导致处于水利尿状态的布拉特洛维大鼠的无溶质水生成受到部分抑制,以及通过输注抗利尿激素使大鼠处于最大抗利尿状态时的无溶质水重吸收受到部分抑制。在这两种情况下,抑制程度都不如注射引起类似利钠反应剂量的呋塞米后观察到的那样显著。大剂量呋塞米会阻断对心房提取物的利钠反应,而当通过大量输注生理盐水产生相当水平的钠和水输出时,对心房提取物的利钠反应会增强。有人提出,心房利钠因子可能会抑制髓袢升支粗段以外的肾单位段中的钠转运。呋塞米也可能作用于相同的肾小管部位或抑制心房利钠因子的肾小管分泌。