Sonnenberg H
Department of Physiology, University of Toronto, Ont., Canada.
Can J Physiol Pharmacol. 1987 Oct;65(10):2021-3. doi: 10.1139/y87-316.
Following the discovery of the natriuretic effect of atrial extract, our laboratory attempted to dissect the possible physiological role of atrial natriuretic factor. Initial micropuncture experiments demonstrated that the reduction of tubular sodium reabsorption was localized in the medullary collecting duct, a nephron site in which sodium transport was known to be inhibited after acute hypervolemia. Partial removal of the endogenous source of atrial natriuretic factor was associated with a reduced renal response to hypervolemia, confirming that the factor is causally involved in acute sodium balance. In vitro incubation of atrial tissue was used to investigate mechanisms of release of atrial natriuretic factor. It was found that agonists known to activate the intracellular polyphosphoinositide system in other tissues were effective in releasing natriuretic activity from the atria into the incubation medium. To determine whether atrial natriuretic factor might play a role in hypertension, atrial natriuretic content was measured in spontaneously hypertensive rats and their normotensive controls. Hypertension was associated with increased content. Since the renal response to exogenous factor was not impaired in these animals, we suggested that the increased content might play a compensatory role. Our early studies thus indicated that atrial natriuretic factor was a previously unrecognized hormone involved in cardiovascular regulation.
在发现心房提取物的利钠作用之后，我们实验室试图剖析心房利钠因子可能的生理作用。最初的微穿刺实验表明，肾小管钠重吸收的减少定位于髓质集合管，这是一个已知在急性血容量过多后钠转运受抑制的肾单位部位。部分去除心房利钠因子的内源性来源与肾脏对血容量过多的反应减弱相关，证实该因子与急性钠平衡有因果关系。利用心房组织的体外孵育来研究心房利钠因子的释放机制。发现已知能激活其他组织中细胞内多磷酸肌醇系统的激动剂可有效地将心房利钠活性释放到孵育培养基中。为了确定心房利钠因子是否可能在高血压中起作用，对自发性高血压大鼠及其正常血压对照大鼠的心房利钠含量进行了测量。高血压与心房利钠含量增加相关。由于这些动物对外源性因子的肾脏反应未受损，我们认为心房利钠含量增加可能起代偿作用。因此，我们早期的研究表明，心房利钠因子是一种以前未被认识的参与心血管调节的激素。
