Mechanism of effect of hypoxia on renal water excretion.
Mechanism of effect of hypoxia on renal water excretion.
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缺氧影响肾水排泄的机制。
DOI：
10.1172/jci109188
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发表时间：
1978
期刊：
影响因子：
--
通讯作者：
K. McDonald
中科院分区：
文献类型：
--
作者：
R. Anderson;R. Pluss;A. S. Berns;J. Jackson;P. Arnold;R. Schrier;K. McDonald
在进行水利尿的麻醉犬中，研究了将氧压从80降至34 mm Hg的效果。这种缺氧程度与抗利尿有关，尿渗透压（Uosm）从107增加到316 mumol /kg H(2)O (P < 0.001)，血浆精氨酸加压素从0.06增加到7.5 muU/ml （P < 0.05）。然而，缺氧与心输出量（CO，从4.2到4.7升/分钟）、平均动脉压（MAP，从143到149毫米汞柱）、肾小球滤过率（GFR，从46到42毫升/分钟）、溶质排泄率（SV，从302到297莫摩尔/分钟）或滤过分数（从0.26到0.27，NS）的显著变化无关。缺氧与肾血管阻力增加相关（从0.49到0.58 mm Hg/ml / min, P < 0.01）。缺氧诱导的抗利尿作用在神经支配肾和去神经支配肾中是相同的。为了进一步研究加压素在抗利尿中的作用，我们在去垂体动物中诱导了缺氧。缺氧对去垂体动物的CO、MAP、GFR、SV和肾血流量的影响与正常动物相同。然而，与完整动物相比，缺氧对垂体切除动物没有显著的抗利尿作用（uosl从72到82 mosmol/kg H(2)O）。为了描述缺氧刺激的抗利尿激素释放的传入通路，在化学或压力感受器去神经的狗中诱导缺氧。缺氧对去神经动物CO、MAP、GFR、SV和肾血流量的影响与非去神经动物相同。缺氧导致化学感受器（Uosm为113 ~ 357 mosmol/kg H(2)O, P < 0.001）失神经动物的抗利尿，而压力感受器（Uosm为116 ~ 138 mosmol/kg H(2)O， NS）无抗利尿作用。为了确定低氧是否会改变肾对抗利尿激素的反应，我们将外源性抗利尿激素给予正常氧合组和低氧组的狗。抗利尿作用在两组间无明显差异。这些结果表明，缺氧诱导的抗利尿作用不依赖于CO、MAP、SV、滤过分数、肾神经或肾对抗利尿素的反应的改变，并通过压力受体介导的抗利尿素释放发生。压力感受器刺激的性质仍有待阐明。
The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H(2)O (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 muU/ml, (P < 0.05). However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H(2)O). To delineate the afferent pathway for hypoxia-stimulated vasopressin release, hypoxia was induced in dogs with either chemo- or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H(2)O, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H(2)O, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was administered to normoxic and hypoxic groups of dogs. The antidiuretic effect of vasopressin was no different in these two groups. These results demonstrate that hypoxia induces an antidiuresis which is independent of alterations in CO, MAP, SV, filtration fraction, renal nerves, or renal response to vasopressin and occurs through baroreceptor-mediated vasopressin release. The nature of the baroreceptor stimulation remains to be elucidated.