Kunes J, Nedvídek J, Zicha J
Institute of Physiology, Czechoslovak Academy of Sciences, Prague.
J Hypertens Suppl. 1989 Dec;7(6):S204-5. doi: 10.1097/00004872-198900076-00098.
The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. Vasopressin-deficient, vasopressin-synthesizing and vasopressin-deficient rats chronically supplemented with deamino-8-D-arginine vasopressin (dDAVP) were compared with water-drinking controls. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. The development of DOCA-salt hypertension was attenuated in the vasopressin-deficient rats, which had a similar level of total body water, slightly increased intracellular water and significantly decreased extracellular fluid volume compared with the hypertensive vasopressin-synthesizing rats. Consequently, in the vasopressin-deficient rats, the ratio of extracellular fluid volume to intracellular water did not differ from that of controls. A vasopressin deficiency was associated with a failure to expand the interstitial fluid volume although plasma volume was increased. Unaltered total body water together with elevated plasma osmolality indicated an extracellular water deficiency in DOCA-salt-treated vasopressin-deficient rats. Chronic dDAVP supplementation restored the body fluid pattern and the hypertensive response of the DOCA-salt-treated vasopressin-deficient rats. In conclusion, the antidiuretic effects of vasopressin are necessary for the interstitial fluid volume expansion that is essential for a full development of DOCA-salt hypertension.
在年轻的布拉特洛维大鼠中研究了血管加压素在调节机体水容量及其在血管内、间质和细胞内区间分布中的作用，以及特定机体水区间在去氧皮质酮盐性高血压发病机制中的重要性。将血管加压素缺乏、血管加压素合成以及长期补充去氨基-8-D-精氨酸血管加压素（dDAVP）的血管加压素缺乏大鼠与饮水对照组进行比较。慢性去氧皮质酮盐处理使血管加压素合成动物出现明显高血压；在这些动物中，由于细胞外液体积扩张，机体水略有增加，而细胞内水趋于减少，因此细胞外液体积与细胞内水的比值显著升高。与高血压血管加压素合成大鼠相比，血管加压素缺乏大鼠的去氧皮质酮盐性高血压发展减弱，其总体水水平相似，细胞内水略有增加，细胞外液体积显著减少。因此，在血管加压素缺乏大鼠中，细胞外液体积与细胞内水的比值与对照组无差异。尽管血浆容量增加，但血管加压素缺乏与间质液体积未能扩张有关。去氧皮质酮盐处理的血管加压素缺乏大鼠总体水不变但血浆渗透压升高表明细胞外水缺乏。长期补充dDAVP可恢复去氧皮质酮盐处理的血管加压素缺乏大鼠的体液模式和高血压反应。总之，血管加压素的抗利尿作用对于间质液体积扩张是必需的，而间质液体积扩张对于去氧皮质酮盐性高血压的充分发展至关重要。
