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钙在大鼠器官培养中抗利尿激素渗透和非渗透释放中的作用

Role of calcium in osmotic and nonosmotic release of vasopressin from rat organ culture.

作者信息

Ishikawa S, Schrier R W

出版信息

Am J Physiol. 1983 May;244(5):R703-8. doi: 10.1152/ajpregu.1983.244.5.R703.

DOI:10.1152/ajpregu.1983.244.5.R703
PMID:6405631
Abstract

In the present study the role of calcium (Ca) in the stimulation of arginine vasopressin (AVP) release from the cultured rat hypothalamoneurohypophyseal complex (HNC) was examined in response to three different stimuli, 56 mM potassium chloride, an increase in medium osmolality from 290 to 310 mosmol/kg H2O, or 1 X 10(-6) M angiotensin II (ANG II). With all three stimuli AVP release from rat HNC explants was enhanced by increasing Ca concentration in the medium from 0 to 1.8 mM Ca. However, high concentrations of Ca (8 mM) inhibited the response of AVP release to either hyperosmolality or angiotensin II. Chemically dissimilar blockers of cellular Ca uptake, verapamil (5.2 X 10(-6) or 5.2 X 10(-5) M) or nifedipine (5.8 X 10(-6) or 5.8 X 10(-5) M), completely abolished AVP release from rat HNC explants in response to the three different stimuli in 1.8 mM Ca. In a normal concentration of medium Ca (1.8 mM) a Ca ionophore, A23187 (3.8 X 10(-5) M), significantly enhanced the osmotic and nonosmotic (ANG II-stimulated) release of AVP from rat HNC explants compared with controls without Ca ionophore. This effect of Ca ionophore to enhance AVP release was more evident in a lower Ca medium (0.9 mM Ca in the hyperosmolality study and 0.3 mM Ca in the ANG II study). These results therefore indicate that cellular Ca uptake is an important modulator of osmotic and nonosmotic AVP release from the intact rat hypothalamoneurohypophyseal system. The influence of extracellular Ca on the osmotic and nonosmotic release of AVP is also demonstrated.

摘要

在本研究中,检测了钙(Ca)在刺激培养的大鼠下丘脑神经垂体复合体(HNC)释放精氨酸加压素(AVP)中的作用,该刺激是针对三种不同的刺激因素,即56 mM氯化钾、培养基渗透压从290 mosmol/kg H₂O升高至310 mosmol/kg H₂O,或1×10⁻⁶ M血管紧张素II(ANG II)。对于所有这三种刺激因素,通过将培养基中的钙浓度从0 mM增加至1.8 mM,大鼠HNC外植体的AVP释放均得到增强。然而,高浓度的钙(8 mM)会抑制AVP释放对高渗或血管紧张素II的反应。细胞钙摄取的化学性质不同的阻滞剂,维拉帕米(5.2×10⁻⁶或5.2×10⁻⁵ M)或硝苯地平(5.8×10⁻⁶或5.8×10⁻⁵ M),在1.8 mM钙的情况下,完全消除了大鼠HNC外植体对三种不同刺激因素的AVP释放。在正常浓度的培养基钙(1.8 mM)中,与无钙离子载体的对照组相比,钙离子载体A23187(3.8×10⁻⁵ M)显著增强了大鼠HNC外植体中AVP的渗透和非渗透(ANG II刺激)释放。钙离子载体增强AVP释放的这种作用在较低钙浓度的培养基中更为明显(在高渗研究中为0.9 mM钙,在ANG II研究中为0.3 mM钙)。因此,这些结果表明细胞钙摄取是完整大鼠下丘脑神经垂体系统中AVP渗透和非渗透释放的重要调节因子。同时也证明了细胞外钙对AVP渗透和非渗透释放的影响。

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