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首页> 外文期刊>American Journal of Physiology >Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension.
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Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension.

机译：遗传性AVP缺乏症消除了感冒引起的利尿，但并未减轻感冒引起的高血压。

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Chronic cold exposure causes hypertension and diuresis. The aim of this study was to determine whether vasopressin (AVP) plays a role in cold-induced hypertension and diuresis. Two groups of Long-Evans (LE) and two groups of homozygous AVP-deficient Brattleboro (VD) rats were used. Blood pressure (BP) was not different among the four groups during a 2-wk control period at room temperature (25 degrees C, warm). After the control period, one LE group and one VD group were exposed to cold (5 degrees C); the remaining groups were kept at room temperature. BP and body weight were measured weekly during exposure to cold. Food intake, water intake, urine output, and urine osmolality were measured during weeks 1, 3, and 5 of cold exposure. At the end of week 5, all animals were killed and blood was collected for measurement of plasma AVP. Kidneys were removed for measurement of renal medulla V2 receptor mRNA and aquaporin-2 (AQP-2) protein expression. BP of LE and VD rats increased significantly by week 2 of cold exposure and reached a high level by week 5. BP elevations developed at approximately the same rate and to the same degree in LE and VD rats. AVP deficiency significantly increased urine output and solute-free water clearance and decreased urine osmolality. Chronic cold exposure increased urine output and solute-free water clearance and decreased urine osmolality in LE rats, indicating that cold exposure caused diuresis in LE rats. Cold exposure failed to affect these parameters in VD rats, suggesting that the AVP system is responsible for cold-induced diuresis. Cold exposure did not alter plasma AVP in LE rats. Renal medulla V2 receptor mRNA and AQP-2 protein expression levels were decreased significantly in the cold-exposed LE rats, suggesting that cold exposure inhibited renal V2 receptors and AVP-inducible AQP-2 water channels. We conclude that 1) AVP may not be involved in the pathogenesis of cold-induced hypertension, 2) the AVP system plays a critical role in cold-induced diuresis, and 3) cold-induced diuresis is due to suppression of renal V2 receptors and the associated AQP-2 water channels, rather than inhibition of AVP release.
机译：慢性冷暴露会导致高血压和利尿。这项研究的目的是确定血管加压素（AVP）是否在感冒诱发的高血压和利尿中起作用。使用两组Long-Evans（LE）和两组纯合AVP缺陷的Brattleboro（VD）大鼠。在室温（25摄氏度，温暖）下的2周控制期内，四组的血压（BP）均无差异。对照期后，一组LE组和一组VD组暴露于寒冷（5摄氏度）;其余组保持在室温下。在暴露于寒冷期间每周测量一次BP和体重。在冷暴露的第1、3和5周期间测量食物摄入量，水摄入量，尿量和尿渗透压。在第5周结束时，杀死所有动物并收集血液用于血浆AVP的测量。取出肾脏以测量肾髓质V2受体mRNA和水通道蛋白2（AQP-2）蛋白的表达。 LE和VD大鼠的BP在冷暴露的第2周显着增加，并在第5周达到高水平。在LE和VD大鼠中，BP升高的速度大致相同，程度相同。 AVP缺乏会显着增加尿量和无溶质水清除率，并降低尿渗透压。慢性冷暴露增加了LE大鼠的尿量和无溶质的水清除率，降低了尿渗透压，表明冷暴露引起LE大鼠的利尿。寒冷暴露未能影响VD大鼠的这些参数，表明AVP系统是引起寒冷诱导的利尿的原因。冷暴露并没有改变LE大鼠的血浆AVP。在冷暴露的LE大鼠中，肾髓质V2受体mRNA和AQP-2蛋白表达水平显着降低，表明冷暴露抑制了肾V2受体和AVP诱导的AQP-2水通道。我们得出的结论是：1）AVP可能不参与感冒引起的高血压的发病机制; 2）AVP系统在感冒引起的利尿作用中起关键作用; 3）感冒引起的利尿作用是由于肾脏V2受体的抑制和相关的AQP-2水通道，而不是抑制AVP释放。

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