Baylis P H, Zerbe R L, Robertson G L
J Clin Endocrinol Metab. 1981 Nov;53(5):935-40. doi: 10.1210/jcem-53-5-935.
Insulin-induced hypoglycemia causes an increase in plasma vasopressin concentration in man and rat. To assess the mechanism by which this occurs, the effect of hypoglycemia was studied in healthy adults. After insulin injection, a 7-fold rise in plasma immunoreactive arginine vasopressin to 8.2 +/- 3.6 pg/ml was observed in 10 normal subjects. This was associated with a rise in plasma sodium of 2 meq/liter, but no significant change in mean arterial pressure or hematocrit was observed. The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. His plasma vasopressin rose from 1.6 to 12.5 pg/ml with no fall in blood pressure or volume. beta-Adrenergic blockade with propranolol before repeat insulin-induced hypoglycemia did not reduce the vasopressin response (peak plasma vasopressin, 8.1 +/- 1.7 pg/ml), despite suppression of PRA. Linear regression analysis showed that the rise in plasma vasopressin and the percentage decline in plasma glucose correlated significantly (r = 0.57, P less than 0.001). In conclusion, hypoglycemia releases vasopressin nonosmotically by a mechanism that appears to be independent of factors currently known to effect vasopressin secretion.
胰岛素诱导的低血糖会导致人和大鼠血浆血管加压素浓度升高。为了评估其发生机制，我们对健康成年人进行了低血糖影响的研究。在10名正常受试者中，注射胰岛素后，血浆免疫反应性精氨酸血管加压素升高了7倍，达到8.2±3.6 pg/ml。这与血浆钠浓度每升升高2 meq相关，但平均动脉压或血细胞比容未见显著变化。通过观察一名先前显示对渗透压刺激选择性丧失血管加压素反应的患者对低血糖的血管加压素反应，评估了血浆钠升高的意义。他的血浆血管加压素从1.6 pg/ml升至12.5 pg/ml，血压和血容量均未下降。在重复胰岛素诱导的低血糖之前用普萘洛尔进行β-肾上腺素能阻断，尽管抑制了肾素活性，但并未降低血管加压素反应（血浆血管加压素峰值为8.1±1.7 pg/ml）。线性回归分析显示，血浆血管加压素的升高与血浆葡萄糖的下降百分比显著相关（r = 0.57，P < 0.001）。总之，低血糖通过一种似乎独立于目前已知影响血管加压素分泌的因素的机制非渗透性地释放血管加压素。
