Inhibition of nitric oxide facilitates LH release from rat pituitaries.
Inhibition of nitric oxide facilitates LH release from rat pituitaries.
复制标题
抑制一氧化氮促进大鼠垂体释放 LH。
DOI：
10.1016/s0024-3205(97)00356-1
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发表时间：
1997
期刊：
影响因子：
6.1
通讯作者：
Yallampalli,C
中科院分区：
文献类型：
--
作者：
Chatterjee,S;Collins,TJ;Yallampalli,C
我们研究了一氧化氮（NO）调节剂对大鼠垂体LH含量在体内的影响，并研究了它们对LHRH刺激的LH分泌在体外卵巢切除成年雌性Sprague道利大鼠。将Alzet微型泵（流速10 μl/h）递送生理盐水（组I）、1.2mg硝酸甘油（NO供体）（组II）或50 mg硝基-L-精氨酸甲酯（NO合酶（NOS）抑制剂）（组III）皮下植入实验动物。36小时输注后，取出垂体，冷冻用于LH定量，或在灌流系统中以90分钟间隔用10分钟LHRH脉冲（1 ng/ml）破碎并激发10小时。用放射免疫法测定垂体匀浆和每10分钟收集的灌流液中LH的含量。与组I（215.6 ± 5.5 ng; p < 0.04）或组II（221.2 ± 14.9 ng; p < 0.01）相比，组III（150.3 ± 18.6 ng）中的垂体LH水平显著较低，表明低水平的NO刺激体内LH分泌。垂体LH含量在组I和组II中无显著差异。体外研究表明，外源性LHRH刺激反应，测量为平均脉冲反应，Ⅲ组灌流后90分钟内LH释放量为290 ± 23.6ng，灌流10小时内LH释放量为1646.7 ± 270.8ng; I组为57.9 ± 3.1和344.7 ± 24.3 ng，II组为105.3 ± 6.3和633.7 ± 77.1 mg。因此，我们的体外研究表明，与组I和组II相比，组III中LHRH刺激的LH分泌显著增强（p < 0.05），而组II显示出比组I更高的反应性（p < 0.05）。目前的研究结果提供了证据，NOS抑制促进垂体LH分泌。3组对LHRH刺激的LH分泌的不同反应表明NO可能在调节垂体LHRH受体浓度中起作用。然而，这将需要进一步的研究来检验。
We examined the effects of nitric oxide (NO) modulators on rat pituitary LH content in vivo and studied their response to LHRH-stimulated LH secretion in vitro in ovariectomized adult female Sprague Dawley rats. Alzet mini pumps (flow rate 10 μl/h) delivering either normal saline (Group I), 1.2 mg nitroglycerin, a donor of NO (Group II) or 50 mg of nitro-L-Arginine methyl ester, a NO synthase (NOS) inhibitor (Group III), were subcutaneously implanted into experimental animals. Following 36 h infusion, pituitaries were removed and either frozen for LH quantitation, or fragmented and challenged in the superfusion system with 10 min pulses of LHRH (1 ng/ml) at 90 min intervals for 10 hours. LH was assayed by radio-immunoassay (RIA) in the homogenates of pituitaries and in aliquots of the superfusate collected every 10 mins. Significantly lower pituitary LH levels were noted in Group III (150.3 ± 18.6 ng) in comparison to Groups I (215.6 ± 5.5 ng; p < 0.04) or II (221.2 ± 14.9 ng; p < 0.01), suggesting that low levels of NO stimulate LH secretion in vivo. The pituitary LH contents were not significantly different in Groups I and II. In vitro studies reveal that exogenous LHRH stimulated response, measured as average pulse response (90 minute period after LHRH), and total LH released during the 10 hour perfusion, was 290 ± 23.6 ng and 1646.7 ± 270.8 ng, respectively, in Group III; 57.9 ± 3.1, and 344.7 ± 24.3 ng in Group I, and 105.3 ± 6.3, and 633.7 ± 77.1 mg in Group II. Thus, our in vitro studies demonstrate significantly enhanced (p < 0.05) LHRH- stimulated LH secretion in Group III in comparison to Groups I and II, while Group II shows higher responsiveness than Group I (p < 0.05). The results of the current studies provide evidence that NOS inhibition facilitates pituitary LH secretion. The differential responses to LHRH-stimulated LH secretion in vitro in the 3 groups suggest a possible role of NO in modulating pituitary LHRH receptor concentrations. However, this will have to be tested by further studies.