Vindrola O, Aloyz R, Ase A, Finkielman S, Nahmod V E
Instituto de Investigaciones Médicas, Sección Sustancias Vasoactivas, Buenos Aires, Argentina.
Endocrinology. 1988 Aug;123(2):810-5. doi: 10.1210/endo-123-2-810.
Adrenal enkephalin and enkephalin-containing peptides were studied during postnatal development in normotensive (WKY) and spontaneously hypertensive rats (SHR). The effect of chronic treatment with the ganglionic blocker chlorisondamine (5 mg/kg) was also assessed. Free enkephalin immunoreactivity and total enkephalin immunoreactivity, as determined by enzymatic digestion of large enkephalin containing fragments, were quantitated in the adrenal glands at 11 days and 7, 16, and 24 weeks of age. Both total and free metenkephalin were significantly diminished in the adrenal of SHR when compared to WKY at all ages tested. The analysis of the chromatographic profile showed that SHR displayed reduced levels of high and low molecular weight materials at 11 days and 16 weeks of age; however intermediate compounds were high in the glands of these animals. Similar increased values for free met-enkephalin were found in adrenals of WKY and SHR after ganglionic blocker treatment, which means that the relative increase was larger in SHR than WKY; while for total enkephalin the relative increase and the concentration reached in SHR was about half of those presented in WKY. These and other results presented suggest that the basic alteration of the adrenal proenkephalin system of SHR may be due to a genetic reduction of proenkephalin levels. Otherwise, the free enkephalin decrease could be related to changes in nervous input to the adrenal gland.
研究了正常血压大鼠（WKY）和自发性高血压大鼠（SHR）出生后发育过程中肾上腺脑啡肽和含脑啡肽的肽类。还评估了用神经节阻滞剂氯异吲哚铵（5毫克/千克）进行慢性治疗的效果。通过对含大的脑啡肽片段进行酶消化测定的游离脑啡肽免疫反应性和总脑啡肽免疫反应性，在11日龄以及7、16和24周龄时对肾上腺进行了定量。在所有测试年龄，与WKY相比，SHR肾上腺中的总甲硫脑啡肽和游离甲硫脑啡肽均显著减少。色谱图谱分析表明，在11日龄和16周龄时，SHR中高分子量和低分子量物质的水平降低；然而，这些动物肾上腺中的中间化合物含量较高。在神经节阻滞剂治疗后，WKY和SHR的肾上腺中游离甲硫脑啡肽的值有类似的增加，这意味着SHR中的相对增加比WKY更大；而对于总脑啡肽，SHR中的相对增加和达到的浓度约为WKY中的一半。这些以及其他呈现的结果表明，SHR肾上腺前脑啡肽系统的基本改变可能是由于前脑啡肽水平的遗传降低。否则，游离脑啡肽的减少可能与肾上腺神经输入的变化有关。
