Takahashi H, Okabayashi H, Suga K, Matsuzawa M, Ikegaki I, Yoshimura M, Ijichi H
Biochem Biophys Res Commun. 1986 Sep 30;139(3):1285-91. doi: 10.1016/s0006-291x(86)80317-5.
Implication of the brain atrial natriuretic polypeptide on the vasopressin release was investigated using rats fed with a high-sodium containing diet. Sodium loading increased not only the blood pressure but also the urinary output of vasopressin significantly. The plasma vasopressin concentration increased about 10 times after the intracerebroventricular injections of angiotensin II. Thereby, magnitude of the response was significantly smaller in the rat fed with a high sodium diet than in rats with the regular-diet. The hypothalamic content of both vasopressin and atrial natriuretic polypeptide was significantly larger in the high-salt group than the regular-salt. The intraventricular injections of atrial natriuretic polypeptide abolished the vasopressin release induced by the intraventricular injections of angiotensin II. These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment.
采用高钠饮食喂养的大鼠，研究了脑钠尿肽对血管加压素释放的影响。钠负荷不仅显著升高了血压，还显著增加了血管加压素的尿量输出。脑室内注射血管紧张素II后，血浆血管加压素浓度增加了约10倍。因此，高钠饮食喂养的大鼠的反应幅度明显小于常规饮食喂养的大鼠。高盐组中血管加压素和脑钠尿肽的下丘脑含量均显著高于常规盐组。脑室内注射脑钠尿肽可消除脑室内注射血管紧张素II诱导的血管加压素释放。这些结果表明，在下丘脑钠负荷增加的大鼠中，血管加压素的产生增加，但其释放相对受到抑制，并且下丘脑脑钠尿肽增加参与了血管加压素释放的抑制以及降低它们的钠食欲以避免高钠环境。
