Boer G J, van Heerikhuize J, van der Woude T P
Netherlands Institute for Brain Research, Amsterdam.
Acta Endocrinol (Copenh). 1988 Apr;117(4):442-50. doi: 10.1530/acta.0.1170442.
The postnatal developmental course of the enhanced OT serum level of the vasopressin-deficient (homozygous) Brattleboro rat was investigated radioimmunochemically together with the response to treatment with Pitressin tannate. Compared with heterozygous Brattleboro (control) pups, in which serum OT appeared to have an adult value from birth onwards (about 10 pmol/l), homozygous rats had approximately 2-fold enhanced OT serum level throughout early development. Between day 55 and adulthood the levels of OT rose further to 40-50 pmol/l. A 3-day treatment with Pitressin tannate both in the period before or after the age (day 16) at which the polyuria of the homozygous Brattleboro mutant can be revealed, failed to reduce the serum OT. It was therefore concluded that the high OT serum levels in the vasopressin-deficient Brattleboro rat are not induced by osmotic imbalance, but probably originates from functional teratological aspects of the mutation.
采用放射免疫化学方法，研究了加压素缺乏型（纯合子）布拉德福德大鼠产后血清催产素（OT）水平升高的发育过程，以及其对鞣酸加压素治疗的反应。与杂合子布拉德福德（对照）幼崽相比，血清OT似乎从出生起就具有成年值（约10 pmol/l），纯合子大鼠在整个早期发育过程中血清OT水平大约提高了2倍。在第55天至成年期之间，OT水平进一步升至40 - 50 pmol/l。在纯合子布拉德福德突变体多尿症可被发现的年龄（第16天）之前或之后，用鞣酸加压素进行为期3天的治疗，均未能降低血清OT水平。因此得出结论，加压素缺乏型布拉德福德大鼠血清OT水平升高并非由渗透失衡引起，而是可能源于该突变的功能性致畸方面。
