Goraca A
Department of Physiology, Institute of Biochemistry, Medical University of Lodz, 90-131 Lodz, Poland.
Endocr Regul. 2000 Sep;34(3):127-34.
It was previously observed that infusion of angiotensin II, hypertonic saline and N-methyl-D-aspartic acid (NMDA) causes an increase in vasopressin and cardiodepressant factor release from the posterior pituitary lobe into the blood (Goraca 1998). The aim of present study was to investigate if the cardiodepressant factor and vasopressin are simultaneously released from the pituitary into the blood dialysate during acute hypoxia.
The samples of dialysates of venous blood outflowing from the vicinity of cavernous sinus of the sella turcica were collected in anaesthetized rats. 30-min hypoxia was obtained by increasing the respiratory dead space. The concentration of vasopressin in blood dialysate was determined by radioimmunoassay, and cardiodepressant activity on spontaneously discharging pacemaker tissue of the right auricle of the right heart atrium.
Acute hypoxia caused simultaneously an increase in cardiodepressant activity and vasopressin concentration in the blood dialysate outflowing from the vicinity of cavernous sinus of the sella turcica.
These data suggest that cardiodepressant factor released together with vasopressin from the posterior pituitary lobe decrease the heart contraction rate and improves coronary circulation affected by vasopressin release.
先前观察到输注血管紧张素II、高渗盐水和N-甲基-D-天冬氨酸（NMDA）会导致血管加压素和心脏抑制因子从垂体后叶释放到血液中增加（戈拉卡，1998年）。本研究的目的是调查在急性缺氧期间，心脏抑制因子和血管加压素是否同时从垂体释放到血液透析液中。
在麻醉的大鼠中收集从蝶鞍海绵窦附近流出的静脉血透析液样本。通过增加呼吸死腔获得30分钟的缺氧。通过放射免疫测定法测定血液透析液中血管加压素的浓度，并测定对右心房右心耳自发放电起搏组织的心脏抑制活性。
急性缺氧导致从蝶鞍海绵窦附近流出的血液透析液中的心脏抑制活性和血管加压素浓度同时增加。
这些数据表明，与血管加压素一起从垂体后叶释放的心脏抑制因子会降低心率，并改善受血管加压素释放影响的冠状动脉循环。
