The relation between carotid solute concentration and renal water excretion in conscious dogs.
The relation between carotid solute concentration and renal water excretion in conscious dogs.
复制标题
清醒犬颈动脉溶质浓度与肾水排泄之间的关系。
DOI：
10.1111/j.1748-1716.1982.tb06950.x
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Zucker,IH
中科院分区：
文献类型：
--
作者：
Dietz,JR;Bie,P;Gilmore,JP;Share,L;Zucker,IH
Verney的假设，大脑的垂体后叶素受体控制肾脏排泄的水通过加压素进行了重新研究，在清醒的训练狗提供了双侧皮肤环含有颈总动脉。在两只狗的多项实验中，双侧颈动脉内注射（0.25 ml. (kg B.重量）-10 s内每动脉1次）的高渗氯化钠溶液（0.257 mol/l）在短暂水利尿期间未能产生抗利尿反应，尽管据估计注射可使颈动脉血的渗透压升高12- 15%。另5只犬双侧颈动脉内注入高渗盐水（45 μmol. (kg B.重量min）-1/动脉，持续10 min）导致颈静脉渗透压升高3%，并出现抗利尿反应，但心率或平均动脉压未出现可检测到的变化。同等的静脉高渗或颈动脉等渗输注与抗利尿反应无关。血浆中加压素的伴随浓度分析不支持以下假设：颈动脉内高渗输注的抗利尿反应完全或主要是由于加压素的释放。尽管外源性加压素可以模拟肾反应。它的结论是，目前的结果，虽然不一致的几个Verney的结果和proptions-yet支持的概念，大脑溶质受体影响肾水排泄率。
Verney's hypothesis of cerebral osmoreceptors controlling the renal excretion of water via vasopressin was reinvestigated in conscious trained dogs provided with bilateral skin loops containing the common carotid arteries. In multiple experiments in two dogs, bilateral intracarotid injections (0.25 ml.(kg b. wt.)‐1per artery in 10 s) of a hyperosmotic solution of sodium chloride (0.257 mol/l) during transient water diuresis failed to produce an antidiuretic response, although it is estimated that the injections elevated the osmolality of the carotid blood by 12–15%. In another 5 dogs, bilateral intracarotid infusions of hyperosmotic saline (45 μmol. (kg b. wt. min)‐1per artery for 10 min) during sustained water diuresis resulted in a 3% increase in jugular venous osmolality and an antidiuretic response without detectable changes in heart rate or mean arterial pressure. Equal intravenous hyperosmotic or intracarotid isosmotic infusions were not associated with antidiuretic responses. Analysis of the concomitant concentrations of vasopressin in plasma fell short of supporting the hypothesis that the antidiuretic response to intracarotid hyperosmotic infusions was exclusively or mainly due to liberation of vasopressin. although the renal response could be mimicked by exogenous vasopressin. It is concluded that the present results—although discordant with several of Verney's results and assumptions—nevertheless support the concept of a cerebral solute receptor influencing the rate of renal water excretion.