Effects of peptides in the hypothalamic vasopressinergic nuclei.

1)下丘脑后叶加压素能核(视上核或室旁核)微量注射毒扁豆碱激动剂奥托莫林可产生明显的抗利尿作用，其作用与血浆加压素水平升高有关。预先微量注射M受体拮抗剂阿托品或静脉注射血管加压素(V1+V2)受体拮抗剂d(CH2)5-D-Tyr(ET)-VAVP可完全阻断上述效应。2)视上核内注射神经肽P物质也有明显的抗利尿作用。在P物质的最大作用下，尿中的加压素浓度增加到对照组的大约26倍。预先微量注射P物质受体拮抗剂Spantide可抑制P物质的抗利尿作用。室旁核微量注射P物质也有明显的抗利尿作用。3)与加压素共存的kappa类阿片肽强啡肽(1-13)在视上核或室旁核注射时，可引起血浆加压素水平升高。预先微量注射纳洛酮可抑制视上注射的作用，但不是侧脑室注射的作用。不与阿片受体结合的强啡肽(2-13)注射到视上核时与强啡肽(1-13)产生的效应基本相同，而对侧脑室旁核注射强啡肽(1-13)的作用要弱于强啡肽(1-13)。结果表明，特定激动剂刺激核团M受体或P物质受体可引起加压素的释放，强啡肽(1-13)通过阿片受体激动室旁核神经元，并通过非阿片受体刺激视上核神经元释放加压素。

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.