Atrial natriuretic factor inhibits dehydration and hemorrhage-induced vasopressin release.
Atrial natriuretic factor inhibits dehydration and hemorrhage-induced vasopressin release.
复制标题
心房钠尿因子抑制脱水和出血引起的加压素释放。
DOI：
10.1159/000124085
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发表时间：
1985
影响因子：
4.1
通讯作者：
Samson,WK
中科院分区：
文献类型：
--
作者：
Samson,WK
心脏来源的肽，称为心房利尿钠因子，具有利钠和利尿的特性，其作用在生理上与抗利尿肽精氨酸加压素（AVP）的作用相反。除了它们在肾脏中的相反作用外，目前的结果表明，这些因子之一，Atriopeptin III，可以抑制大鼠脱水和出血引起的 AVP 释放。 3天禁水导致血浆AVP水平升高（36.1±4.7pg AVP/ml），静脉输注0.02（21.4±3.6）、0.2（15.6±1.6）和2.0（13.9±3.8）nmol Atriopeptin III后显着降低。此外，2.0 nmol Atriopeptin III 显着降低出血后 AVP 水平 (54.8 ± 13.7) 至接近静息水平的值 (10.2 ± 3.7)。结果表明，心脏肽在控制 AVP 释放中发挥作用，并且存在肽能反调节系统，用于维持体液和电解质稳态。
Peptides of cardiac origin, termed atrial natriuretic factors, possess both natriuretic and diuretic properties, actions which physiologically contradict those of the antidiuretic peptide, arginine vasopressin (AVP). In addition to their opposing actions in the kidney, the present results indicate that one of these factors, Atriopeptin III, can inhibit dehydration and hemorrhage-induced AVP release in the rat. 3 days of water deprivation resulted in elevated plasma AVP levels (36.1 ± 4.7 pg AVP/ml) which were significantly reduced following intravenous infusion of 0.02 (21.4 + 3.6), 0.2 (15.6 ± 1.6), and 2.0 (13.9 ± 3.8) nmol Atriopeptin III. Furthermore, 2.0 nmol Atriopeptin III significantly reduced post-hemorrhage levels (54.8 ± 13.7) of AVP to values that approximated resting levels (10.2 ± 3.7). The results suggest a role for cardiac peptides in the control of AVP release as well as the existence of a counterregulatory system, peptidergic in nature, for the maintenance of fluid and electrolyte homeostasis.