Zhang Y, Morgan T O
Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
Blood Press. 1994 Mar;3(1-2):67-71. doi: 10.3109/08037059409101523.
The role of the macula densa in the control of renin synthesis during sodium depletion was studied in Balb/c mice which had their left kidney made hydronephrotic 6 weeks earlier. The role of the nervous system was studied by giving the mice propranolol or by denervation of the left kidney. There was no net secretion of renin from the left hydronephrotic kidney on control or low sodium diet. All plasma renin came from the right kidney. Sodium depletion caused similar rises in renin content of the normal and hydronephrotic kidney. These rises were accompanied by increases in mRNA for renin in both kidneys. Denervation of the left hydronephrotic kidney caused a fall in renal renin content. However, sodium depletion caused a significant rise in both renin mRNA and renal renin in the control and denervated hydronephrotic kidney. Propranolol decreased the renin content of normal and hydronephrotic kidneys. Sodium depletion caused a rise in mRNA and renal renin in both kidneys although the absolute final amount was less than in the control animals. Sodium depletion stimulates renin synthesis in a normal kidney and a kidney without a macula densa. This response is not affected by the nervous supply to the kidney. In the hydronephrotic mouse subjected to sodium depletion the synthesis and secretion of renin appear to be disassociated.
在6周前左肾造成肾积水的Balb/c小鼠中，研究了致密斑在钠耗竭期间对肾素合成的控制作用。通过给小鼠使用普萘洛尔或去除左肾神经来研究神经系统的作用。在对照饮食或低钠饮食条件下，左肾积水的肾脏没有肾素的净分泌。所有血浆肾素均来自右肾。钠耗竭导致正常肾脏和肾积水肾脏的肾素含量出现类似升高。这些升高伴随着两个肾脏中肾素mRNA的增加。去除左肾积水肾脏的神经导致肾脏肾素含量下降。然而，钠耗竭导致对照和去神经支配的肾积水肾脏中的肾素mRNA和肾脏肾素均显著升高。普萘洛尔降低了正常肾脏和肾积水肾脏的肾素含量。钠耗竭导致两个肾脏中的mRNA和肾脏肾素升高，尽管最终的绝对量低于对照动物。钠耗竭刺激正常肾脏和没有致密斑的肾脏中的肾素合成。这种反应不受肾脏神经供应的影响。在钠耗竭的肾积水小鼠中，肾素的合成和分泌似乎是分离的。
