Role of NO on vasopressin and oxytocin release and blood pressure responses during osmotic stimulation in rats.
Role of NO on vasopressin and oxytocin release and blood pressure responses during osmotic stimulation in rats.
复制标题
NO 对大鼠渗透刺激期间加压素和催产素释放以及血压反应的作用。
DOI：
10.1152/ajpregu.1997.273.3.r1024
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Summy-Long,JY
中科院分区：
文献类型：
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作者：
Kadekaro,M;Liu,H;Terrell,ML;Gestl,S;Bui,V;Summy-Long,JY
将NG-硝基-L-精氨酸甲酯（L-NAME，250 μ g/5 μ l）、一氧化氮（NO）合酶抑制剂或人工脑脊液（5 μ l）脑室内给予清醒的未处理大鼠或皮下注射（15 μ l/kg）NaCl（0.15、0.45或1.0 M）或仅给予针刺的大鼠。侧脑室注射L-NAME增加血浆中的血管加压素（VP）和催产素（OT）在控制幼稚大鼠，表明NO紧张性抑制基础分泌的两种激素在等渗等容条件。高渗盐水（0.45和1.0 M NaCl）的渗透刺激升高了两种激素的血浆水平。中枢阻断NO合成酶进一步增强分泌OT在温和的，但不强，渗透刺激，而高水平的VP仍然不受L-NAME。在用针刺或0.15 M NaCl处理的动物中，L-NAME后仅OT水平增加。因此，NO选择性地抑制OT释放响应于疼痛刺激（针刺）和适度的渗透刺激，以促进VP的优先释放。皮下注射0.15和0.45 M NaCl后观察到短暂的升压反应，但在1.0 M NaCl后获得持续反应。然而，无论动物是否接受NaCl溶液，L-NAME治疗都会升高所有动物的血压。因此，NO诱导的血管舒张维持基础动脉血压并限制对渗透刺激的升压反应。
NG-nitro-L-arginine methyl ester (L-NAME, 250 micrograms/5 microliters), an inhibitor of nitric oxide (NO) synthase, or artificial cerebrospinal fluid (5 microliters) was administered intracerebroventricularly to conscious naive rats or to rats treated subcutaneously (15 microliters/kg) with NaCl (0.15, 0.45, or 1.0 M) or given a needle prick only. Intracerebroventricular injection of L-NAME increased plasma concentration of vasopressin (VP) and oxytocin (OT) in control naive rats, indicating that NO tonically inhibits basal secretion of both hormones during isosmotic isovolemic conditions. Osmotic stimulation with hypertonic saline (0.45 and 1.0 M NaCl) elevated plasma levels of both hormones as expected. Central blockade of NO synthase further enhanced secretion of OT during mild, but not strong, osmotic stimulation, whereas the high levels of VP remained unaffected by L-NAME. In animals treated with the needle prick or 0.15 M NaCl, only OT levels were increased after L-NAME. Therefore, NO selectively inhibits OT release in response to a painful stimulus (needle prick) and moderate osmotic stimulation to promote a preferential release of VP. A transient pressor response was observed after subcutaneous injection of 0.15 and 0.45 M NaCl, but a sustained response was obtained after 1.0 M NaCl. Regardless of whether the animals received NaCl solutions, however, treatment with L-NAME elevated blood pressure in all animals. Thus NO-induced vasodilation maintains basal arterial blood pressure and limits the pressor response to osmotic stimulation.