精氨酸加压素的血管和肾小管效应在大鼠醋酸脱氧皮质酮（DOCA）-盐高血压发展中的作用。
Contribution of vascular and tubular effects of arginine-vasopressin to the development of deoxycorticosterone acetate (DOCA)-salt hypertension in rats.
作者信息
Hofbauer K G, Mah S C, Wood J M, Baum H P, Hänni H, Opperman J R, Kraetz J
出版信息
J Hypertens Suppl. 1984 Dec;2(3):S333-5.
The role of arginine-vasopressin (AVP) in the pathogenesis of deoxycorticosterone acetate (DOCA) salt hypertension in rats was studied with AVP receptor antagonists for its tubular (V2) and/or vascular (V1) actions. When chronic (six weeks) infusion of the antagonists was started concomitantly with DOCA-salt treatment the development of hypertension was attenuated by the V1-antagonist and prevented by the V1V2-antagonist. However, the V1V2-antagonist induced severe and persistent hypernatraemia in all rats. When chronic (two weeks) infusion of the antagonists was started in rats with established hypertension after five weeks of DOCA-salt treatment blood pressure was not influenced by the V1-antagonist. The rats which received the V1V2-antagonist died from hypernatraemia within four days. These results suggest that in DOCA-salt treated rats AVP is essential for the prevention of severe and life-threatening hypernatraemia. AVP appears to contribute significantly to the development of this form of hypertension through both its vascular and tubular effects.
采用精氨酸加压素（AVP）受体拮抗剂，研究了AVP在大鼠醋酸脱氧皮质酮（DOCA）盐性高血压发病机制中的作用，以观察其肾小管（V2）和/或血管（V1）效应。当在DOCA盐治疗的同时开始长期（6周）输注拮抗剂时，V1拮抗剂可减轻高血压的发展，而V1V2拮抗剂可预防高血压的发生。然而，V1V2拮抗剂在所有大鼠中均诱发了严重且持续的高钠血症。当在DOCA盐治疗5周后对已患高血压的大鼠开始长期（2周）输注拮抗剂时，V1拮抗剂对血压无影响。接受V1V2拮抗剂的大鼠在4天内死于高钠血症。这些结果表明，在DOCA盐处理的大鼠中，AVP对于预防严重且危及生命的高钠血症至关重要。AVP似乎通过其血管和肾小管效应，对这种高血压的发展有显著贡献。
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