Sato K, Kimura T, Ota K, Shoji M, Inoue M, Ohta M, Yamamoto T, Funyu T, Yoshinaga K, Abe K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Acta Endocrinol (Copenh). 1993 Jul;129(1):65-74. doi: 10.1530/acta.0.1290065.
To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume receptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volume expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran (9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/l NaCl alone was administered. Plasma AVP and ANH and cardiovascular and renal functions were determined. Hypertonic saline and 9D-HS also were administered into the vagotomized and sham operated dogs, and the same parameters were determined. Mean blood pressure and heart rate never changed in all the groups, but central venous pressure and plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increased slightly but plasma volume never changed. Plasma AVP increased in the order of hypertonic saline, 6D-HS and 9D-HS, but plasma ANH increased in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma ANH. Urine sodium and potassium excretion and urine flow increased in hypertonic saline, 6D-HS and 9D-HS groups, but these increases were comparable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an effect on the suppression of the AVP response to osmotic stimuli, and increased plasma ANH release never potentiated the natriuresis under the hypertonic plasma volume expansion.
为了评估循环心房利钠激素（ANH）在响应血浆容量扩张时，除了容量受体介导的机制外，是否会减弱精氨酸加压素（AVP）对血浆渗透压升高的反应，以及在高渗性血浆容量扩张情况下，血浆AVP和ANH的变化是否会影响肾溶质排泄，将高渗盐水（0.95mol/L盐水）单独、含6%右旋糖酐的高渗盐水（6D-HS）和含9%右旋糖酐的高渗盐水（9D-HS）分别注入麻醉犬体内。在对照研究中，单独注入0.15mol/L NaCl。测定血浆AVP和ANH以及心血管和肾功能。高渗盐水和9D-HS也分别注入迷走神经切断和假手术犬体内，并测定相同参数。所有组的平均血压和心率均未改变，但6D-HS和9D-HS组的中心静脉压和血浆容量显著增加。在对照和高渗盐水组中，中心静脉压略有升高，但血浆容量未改变。血浆AVP升高顺序为高渗盐水、6D-HS和9D-HS，而血浆ANH升高顺序相反。迷走神经切断使对9D-HS的AVP反应恢复到对高渗盐水反应的75%，同时血浆ANH显著升高。高渗盐水、6D-HS和9D-HS组的尿钠和钾排泄以及尿流量增加，但各组间这些增加相当。在对照组中，这些参数未改变。这些结果表明，容量受体介导的迷走神经和ANH对血浆容量扩张的反应可能对抑制AVP对渗透压刺激的反应有影响，并且在高渗性血浆容量扩张情况下，血浆ANH释放增加并未增强利钠作用。
