GROWTH HORMONE REGULATING PEPTIDES IN MONKEY HYPOTHALAMUS

生殖过程中发生的内分泌变化之一 衰老是垂体生长激素(GH)分泌减少。 生长激素的减少在一定程度上是免疫力丧失的原因。 许多老年人的功能、肌肉质量和能量。分泌物 GH的表达主要受两种下丘脑肽的调节，即 生长激素释放激素(GHRH)和生长激素抑制激素(GHIH，或 生长抑素)。假设GHRH和GHRH的平衡 生长抑素的活性决定了血液中生长激素的水平。 然而，人们对这两种多肽是如何改变的知之甚少。 在女性开始绝经期间，或如何以及何时 失衡发生在年长的男性身上。我们的实验室已经研制出一种新型的 活体推拉灌流技术，允许我们收集和 有意识地、自由地测量下丘脑肽的释放 移动的猴子。我们发起了一项研究，在这项研究中，我们首先建立了一个 生长激素释放激素和生长抑素的灵敏放射免疫分析。最小的 用这些方法可以检测到7pg的GHRH和2pg的生长抑素 化验。然后我们准备了推拉式灌注器，8例 并测定雄性猕猴GHRH和GHRH的内源性释放 推拉式灌流前后生长抑素的变化 可乐定，一种β-肾上腺素能受体阻滞剂， 已知能刺激生长激素的分泌。还采集了血液样本 同时进行推拉取样。我们发现基础水平的 GHRH很容易测量，而生长抑素的基础水平 几乎察觉不到。有趣的是，可乐定的给药 最初在没有陪伴的情况下血液中的生长激素水平升高 促性腺激素释放激素增加。然而，在可乐定之后的2小时内，两者 GHRH和GH升高。可乐定诱导的初发 生长激素的释放是生长抑素分泌减少的结果 无法确定，因为它在大脑中的分泌量已经很低。 结果表明，我们已经建立了一个体内系统来 监测青少年生长激素释放激素，并定期监测生长抑素 和年长的猴子。这些化验结果将使我们能够调查 大脑对生长激素分泌调节的年龄相关变化。

One of the endocrine changes that occurs during reproductive senescence is a reduction in pituitary growth hormone (GH) secretion. This decline in GH is responsible in part for the demise of immune function, muscle mass and energy in many older people. The secretion of GH is regulated primarily by two hypothalamic peptides, i.e., GH-releasing hormone (GHRH) and GH-inhibiting hormone (GHIH, or somatostatin). It is hypothesized that the balance of GHRH and somatostatin activities determines the level of GH in the blood. However, very little is known about how the two peptides are altered during the onset of menopause in females or how and when their imbalance occurs in older males. Our laboratory has developed an in vivo push-pull perfusion technique which allows us to collect and measure the release of hypothalamic peptides in conscious, freely moving monkeys. We initiated a study in which we first established a sensitive radioimmunoassay for both GHRH and somatostatin. As little as 7 pg of GHRH and 2 pg of somatostatin can be detected with these assays. We then prepared the push-pull perfusion device in 8 young male monkeys and measured the endogenous release of GHRH and somatostatin in push-pull perfusates before and after the administration of clonidine, a beta-adrenergic receptor blocker which is known to stimulate GH secretion. Blood samples were also obtained simultaneously with push-pull samples. We found that basal levels of GHRH were readily measurable, whereas basal levels of somatostatin were barely detectible. Interestingly, administration of clonidine initially increased GH levels in the blood without accompanied increase in GHRH. However, during the 2 h following clonidine, both GHRH and GH were elevated. Whether the clonidine-induced initial release of GH is the result of a lowering of somatostatin secretion could not be determined due to its already low secretion in the brain. The results suggest that we have established an in vivo system to monitor the release of GHRH, and periodically somatostain, in young and older monkeys. These assays will allow us to investigate the age-related changes in the brain's regulation of GH secretion.