Renal cortical and medullary blood flow responses during water restriction: role of vasopressin.

Renal cortical and medullary blood flow responses during water restriction: role of vasopressin.
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限水期间肾皮质和髓质血流反​​应:加压素的作用。

DOI:
10.1152/ajpregu.1996.270.6.r1257
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发表时间:
1996
期刊:
The American journal of physiology.
影响因子:
--
通讯作者:
CowleyJr,AW
CowleyJr,AW
中科院分区:
--
文献类型:
--
作者:
Franchini,KG;CowleyJr,AW

文献摘要

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在未麻醉的大鼠中进行实验,使用植入光纤和激光多普勒血流测定法确定肾脏区域微循环(皮质、外髓质和内髓质)对 48 小时限水的反应。通过连续髓内注射特异性 V1 受体拮抗剂 d(CH2)5 [Tyr-(Me)2, Ala-NH2]AVP (2ng.kg-1.min-1) 来评估加压素 (AVP) 作为肾区域血液低变化调节剂的作用及其对尿液浓缩能力的贡献。限水 48 小时结束时,内髓血流量减少 34%,而皮质和外髓血流量没有变化。通过拮抗剂的连续间质输注,髓内血流量的下降大大减弱(18%)。 48 小时限水期结束时,血浆 AVP 水平从对照水平 3.4 +/- 1.1 增加至 20.5 +/- 5.4 pg/ml (P < 0.05)。对照组大鼠在限制饮水期间,动脉压略有增加,但显着增加。拮抗剂的输注损害了最大尿液浓缩能力,这一点通过在限水第二天测量到的尿液渗透压低于对照组(1,893 +/- 49 vs. 2,419 +/- 225 mosmol/kg H2O;P < 0.05)来证明。钠和尿素浓度分别下降 20% 和 22%,表明这两者都导致接受拮抗剂的大鼠组中观察到的尿液渗透压降低。我们得出的结论是,限水会导致髓内血流选择性减少,这几乎完全是由内源性释放的 AVP 介导的。 AVP 的这种血管效应有助于肾脏的最大浓缩能力。
Experiments were performed in unanesthetized rats to determine responses to 48 h water restriction of the renal regional microcirculation (cortex, outer medulla, and inner medulla) using implanted optical fibers and laser-Doppler flowmetry. The role of vasopressin (AVP) as a mediator of renal regional blood low changes and its contribution to urinary concentrating ability were assessed by continuous intramedullary interstitial infusion of specific V1 receptor antagonist d(CH2)5 [Tyr-(Me)2, Ala-NH2]AVP (2ng . kg-1 . min-1). Inner medullary blood flow decreased 34% at the end of 48 h of water restriction, whereas cortical and outer medullary flow did not change. This fall in inner medullary blood flow was substantially attenuated (18%) by the continuous interstitial infusion of the antagonist. Plasma AVP levels increased from control levels of 3.4 +/- 1.1 to 20.5 +/- 5.4 pg/ml (P < 0.05) by the end of the 48-h period of water restriction. Arterial pressure increased slightly but significantly during water restriction in the control rats. Infusion of antagonist impaired the maximal urinary concentrating ability, as demonstrated by the lower urine osmolality in this group than in the control group (1,893 +/- 49 vs. 2,419 +/- 225 mosmol/kg H2O; P < 0.05) measured during the second day of water restriction. Sodium and urea concentration decreased 20 and 22%, respectively, indicating that both contributed to the lower urine osmolality observed in the group of rats receiving the antagonist. We conclude that water restriction induces a selective decrease in inner medullary blood flow, which is mediated almost completely by endogenously released AVP. This vascular effect of AVP contributes to the maximum concentrating ability of the kidney.