Effects of peptides in the hypothalamic vasopressinergic nuclei.

1)将毒蕈碱激动剂、氧tremorine微注射到下丘脑抗利尿能核（视上核或室旁核），可引起强效的抗利尿作用，并与血浆抗利尿素水平升高有关。显微注射毒毒碱拮抗剂阿托品或静脉注射加压素（V1+V2）受体拮抗剂d (CH2) 5-D-Tyr (Et) -VAVP可完全阻断抗利尿作用。2)神经肽P物质微注射到视上核后也有较强的抗利尿作用。在P物质的最大作用下，尿中的抗利尿激素浓度增加到控制值的大约26倍。微注射P物质受体拮抗剂spantide抑制P物质的抗利尿作用，P物质微注射到室旁核也显示出有效的抗利尿作用。3)一种与抗利尿激素共定位的kappa型阿片肽，dynorphin(1-13)，当注射到视上核或室旁核时，可引起血浆中抗利尿激素水平的升高。显微前注射纳洛酮可抑制视上注射的作用，但不抑制室旁注射的作用。不与阿片受体结合的Dynophin（2-13）在注入视上核时，与dynorphin（1-13）产生的作用大致相同，而注入室旁核时，其产生的作用远不如dynorphin（1-13）。结果表明，特异性激动剂刺激核内毒碱受体或P物质受体可诱导垂体后叶加压素的释放，dynorphin（1-13）通过阿片受体刺激室旁核神经元，并通过非阿片受体刺激视上核神经元释放垂体后叶加压素。

1) Muscarinic agonist, oxotremorine microinjected into the hypothalamic vasopressinergic nucleus (the supraoptic nucleus or the paravetricular nuleus) induced potent antidiuretic effects which were associated with increases in the level of plasma vasopressin. The antidiuretic effects were completely blocked by premicroinjection of muscarinic antagonist, atropine or by preteartment with intravenous injection of vasopressin (V1+V2) receptor antagonist, d (CH2) 5-D-Tyr (Et) -VAVP.2) Neuropeptide, substance P also caused potent antidiuretic effects, when microinjected into the supraoptic nucleus. At the maximal effects of substance P, vasopressin concentration in the urine increased up to approximately 26-fold the control value. Premicroinjection of substance P receptor antagonist, spantide inhibited the antidiuretic effects of substance P. Substance P microinjected into the paraventricular nucleus also demonstrated potent antidiuretic effects.3) A kappa-type opioid peptide, dynorphin (1-13) which colocalizes with vasopressin induced potent antidiuretic effects which accompanied in-creases in the plasma level of vasopressin, when injected into the supraoptic nucleus or the paraventricular nucleus. The effects of the supraoptic injection were inhibited by premicroinjection of naloxone, but were not the effects of the paraventricular injection. Dynophin (2-13) which does not bind to opioid receptors induced approximately equipotent effects to dynorphin (1-13) when injected in the supraoptic nucleus, and it induced much less potent effects than dynorphin (1-13), when injected into the paravetricular nucleus.The results indicate that the stimulation of muscarinic or substance P -receptors in the nuclei by specific agonists induced the release of vasopressin, and that dynorphin (1-13) stimulated the neurons in the paraventricular nucleus through opioid receptors and it stimulated neurons in the supraoptic nucleus via non-opioid receptors, to release vasopressin.