Chabrier P E, Roubert P, Longchamps M O, Plas P, Braquet P
Institut Henri Beaufour Research Laboratories, Les Ulis, France.
J Hypertens Suppl. 1988 Dec;6(4):S290-1. doi: 10.1097/00004872-198812040-00089.
Atrial natriuretic factor (ANF) and angiotensin II (Ang II) appear to act as physiological antagonists in the regulation of blood pressure and fluid homeostasis. After 18 h incubation in cultured vascular smooth muscle cells, Ang II (10(-8) mol/l) induced down-regulation of ANF receptors (reduced by 60% of total binding capacity) that was inhibited by Sar1-Ile8-Ang II (10(-7) mol/l), whereas ANF (10(-8), 10(-7) mol/l) was not able to affect Ang II receptors. The down-regulation provoked by Ang II was associated with an enhancement of ANF-stimulated cyclic (c) GMP formation and was confined to the non-guanylate cyclase-coupled ANF receptor subtype. This suggests that the decrease in ANF receptors elicited by Ang II and the paradoxical increase in the biological activity of ANF may represent a mechanism that represses excessive or long-term pressor effects of Ang II.
心房利钠因子（ANF）和血管紧张素II（Ang II）在血压调节和体液平衡中似乎起着生理性拮抗剂的作用。在培养的血管平滑肌细胞中孵育18小时后，Ang II（10^(-8) mol/l）诱导ANF受体下调（总结合能力降低60%），而Sar1-Ile8-Ang II（10^(-7) mol/l）可抑制这种下调，而ANF（10^(-8)、10^(-7) mol/l）不能影响Ang II受体。Ang II引起的下调与ANF刺激的环磷鸟苷（c）GMP形成增强有关，且仅限于非鸟苷酸环化酶偶联的ANF受体亚型。这表明，Ang II引起的ANF受体减少以及ANF生物活性的反常增加可能代表一种抑制Ang II过度或长期升压作用的机制。
