Ma L Y, McEwen B S, Sakai R R, Schulkin J
Department of Biology, University of Pennsylvania, Philadelphia 19104.
Horm Behav. 1993 Jun;27(2):240-50. doi: 10.1006/hbeh.1993.1018.
We confirm and extend the finding that glucocorticoids facilitate mineralocorticoid-induced sodium intake in the rat. First, we report that subcutaneous injections of dexamethasone (DEX) increase deoxycorticosterone-induced sodium intake. Second, we demonstrate that continuous intravenous infusions of either DEX or corticosterone or the TYPE II glucocorticoid receptor agonist RU28362 increases the sodium intake of aldosterone-treated rats. And third, we measured urine sodium loss and found that rats were in positive sodium balance while receiving aldosterone and the glucocorticoid agonist, suggesting that the increased intake of sodium was primary to renal sodium loss. When taken together with the fact that glucocorticoids can increase the TYPE I aldosterone-preferring receptor population in the brain, the results suggests a role for the glucocorticoid hormones in the arousal of sodium appetite in the rat.
糖皮质激素可促进大鼠体内盐皮质激素诱导的钠摄取。首先，我们报告皮下注射地塞米松（DEX）可增加脱氧皮质酮诱导的钠摄取。其次，我们证明持续静脉输注DEX、皮质酮或II型糖皮质激素受体激动剂RU28362可增加醛固酮处理大鼠的钠摄取。第三，我们测量了尿钠排泄，发现大鼠在接受醛固酮和糖皮质激素激动剂时处于正钠平衡状态，这表明钠摄取增加是肾钠排泄增加的主要原因。结合糖皮质激素可增加大脑中I型醛固酮偏好受体数量这一事实，结果表明糖皮质激素在激发大鼠钠食欲方面发挥作用。
