Kaczmarczyk G, Christe W, Mohnhaupt R, Reinhardt H W
Pflugers Arch. 1983 Feb;396(2):101-5. doi: 10.1007/BF00615512.
In order to quantitate the contribution of the antidiuretic hormone (ADH) to the diuresis of left atrial distension 52 experiments have been performed in 12 conscious, chronically instrumented beagle dogs. Left atrial pressure was increased by a reversible mitral stenosis by about 10 cm H2O (1.0 kPa) for 60 min. Plasma ADH concentration (range between 1.3 and 6.0 pg . ml-1) (radioimmunoassay) decreased in every experiment, the average decrease being about 50%. An i.v. infusion of vasopressin (0.05 mU . min-1 . kg-1) abolished the diuretic effect of left atrial distension or decreased the urine volume below control values; natriuresis was not affected. The magnitude of the vasopressin effect was dependent on the concurrent sodium excretion: when sodium excretion was low during left atrial distension, vasopressin was more effective in reducing the urine volume than when sodium excretion was high. It is concluded that the diuresis of left atrial distension is mediated (a) by a suppression of ADH and (b) by factors controlling sodium excretion, the contribution of these two mechanisms being dependent on the concurrent sodium excretion.
为了定量抗利尿激素(ADH)对左心房扩张利尿作用的贡献,在12只清醒、长期植入仪器的比格犬身上进行了52次实验。通过可逆性二尖瓣狭窄使左心房压力升高约10 cm H2O(1.0 kPa),持续60分钟。每次实验中,血浆ADH浓度(通过放射免疫测定,范围在1.3至6.0 pg·ml-1之间)均下降,平均下降约50%。静脉输注血管加压素(0.05 mU·min-1·kg-1)消除了左心房扩张的利尿作用,或使尿量降至对照值以下;钠排泄未受影响。血管加压素作用的大小取决于同时的钠排泄情况:当左心房扩张期间钠排泄较低时,血管加压素在减少尿量方面比钠排泄较高时更有效。得出的结论是,左心房扩张的利尿作用由(a)ADH的抑制和(b)控制钠排泄的因素介导,这两种机制的贡献取决于同时的钠排泄情况。