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血管紧张素在器官培养的大鼠下丘脑 - 神经垂体系统中对血管加压素释放的渗透调节作用。

Role of angiotensin in the osmotic control of vasopressin release by the organ-cultured rat hypothalamo-neurohypophyseal system.

作者信息

Sladek C D, Joynt R J

出版信息

Endocrinology. 1980 Jan;106(1):173-8. doi: 10.1210/endo-106-1-173.

Abstract

Angiotensin II (AII) appears to either mediate or modulate osmotically stimulated vasopressin (VP) release by the organ-cultured rat hypothalamo-neurohypophyseal system. Saralasin, an AII antagonist, blocked VP release in response to a 10-mosmol increment in culture medium osmolality achieved by the addition of NaCl. This was observed at all concentrations tested (10(-7), 10(-6), 10(-4) M). Saralasin (10(-4) M) also blocked VP release in response to a comparable mannitol-induced increase in osmolality. Since nicotinic-cholinergic antagonists previously were shown to inhibit osmotically stimulated VP release, the effect of hexamthonium, a nicotinic, a nicotinic-cholinergic antagonist, on AII-stimulated VP release was examined. Hexamethonium (10(-5)-10(-3) M) was ineffective in blocking AII stimulation of VP release. This finding coupled with the previous observation that saralasin does not block acetylcholine stimulation of VP release suggests independent AII and cholinergic mechanisms controlling VP release; however, the effectiveness of both types of antagonists in blocking osmotically stimulated VP release indicates some interaction between these regulators of VP release.

摘要

血管紧张素II(AII)似乎通过器官培养的大鼠下丘脑-神经垂体系统介导或调节渗透压刺激的血管加压素(VP)释放。沙拉新是一种AII拮抗剂,可阻断因添加NaCl使培养基渗透压增加10毫渗摩尔而引起的VP释放。在所有测试浓度(10⁻⁷、10⁻⁶、10⁻⁴ M)下均观察到这种情况。沙拉新(10⁻⁴ M)也可阻断因甘露醇诱导的渗透压类似增加而引起的VP释放。由于先前已证明烟碱型胆碱能拮抗剂可抑制渗透压刺激的VP释放,因此研究了烟碱型胆碱能拮抗剂六甲铵对AII刺激的VP释放的影响。六甲铵(10⁻⁵ - 10⁻³ M)无法有效阻断AII对VP释放的刺激。这一发现与先前观察到的沙拉新不会阻断乙酰胆碱对VP释放的刺激相结合,表明存在独立的AII和胆碱能机制控制VP释放;然而,这两种拮抗剂在阻断渗透压刺激的VP释放方面的有效性表明这些VP释放调节因子之间存在某种相互作用。

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