Hamet P, Tremblay J
Clinical Research Institute of Montreal, Quebec.
Clin Invest Med. 1989 Oct;12(5):329-35.
The discovery of atrial natriuretic factor (ANF) constitutes a major advance in our knowledge of negative cell regulatory pathways leading to vasodilation. The biochemical mechanisms of the action of ANF at the cellular level appear to be mediated by the cGMP- particulate guanylate cyclase system. In the kidney, the main cGMP increasing effect of ANF occurs at the level of the glomeruli, but it appears that action of ANF at the lowest part of the distal tubule is required for its natriuretic activity. Although most current knowledge concerning ANF has been obtained with pharmacological doses of the hormone, it appears that endogenous manipulations of ANF, such as those occurring with postural change, are associated with physiological consequences including increases of cGMP, natriuresis, and diuresis. In both experimental and human hypertension, increased plasma levels of ANF are secondary to higher blood pressure. In hypertension, the administration of ANF leads to an exaggerated renal response. We propose as a hypothesis that an abnormality in the expression of a vasodilatory system, such as ANF-cGMP, may play a role in the pathogenesis of hypertension.
心房利钠因子（ANF）的发现是我们在导致血管舒张的负性细胞调节途径知识方面的一项重大进展。ANF在细胞水平上的作用的生化机制似乎是由cGMP - 颗粒型鸟苷酸环化酶系统介导的。在肾脏中，ANF增加cGMP的主要作用发生在肾小球水平，但似乎ANF在远端小管最低部分的作用对于其利钠活性是必需的。尽管目前关于ANF的大多数知识是通过激素的药理剂量获得的，但似乎内源性ANF的变化，如体位改变时发生的变化，与包括cGMP增加、利钠和利尿在内的生理后果有关。在实验性高血压和人类高血压中，ANF血浆水平升高是血压升高的继发结果。在高血压中，给予ANF会导致肾脏反应过度。我们提出一个假设，即血管舒张系统如ANF - cGMP的表达异常可能在高血压的发病机制中起作用。
