Baines A D
Kidney Int. 1982 Feb;21(2):316-22. doi: 10.1038/ki.1982.24.
My study was designed to measure the effect of salt intake on secretion and catabolism of catecholamines by the kidney and renal nerve contributions to urinary catecholamine excretion. Rats with one chronically denervated (DEN) and one innervated (INN) kidney were fed either high salt (HS) or low salt (LS) diets for 5 to 14 days. Under Inactin anesthesia rats were expanded with isotonic saline while LS rats received 10% mannitol to produce the same urine flow rates. Epinephrine excretion was ten times greater from LS than from HS rats; however, epinephrine/inulin excretion was the same from INN and DEN kidneys. Norepinephrine/inulin excretion was 30% less from DEN than from INN kidneys in both HS and LS rats (P less than 0.01). Dopamine/inulin excretion was 20% less from the DEN kidney than from the INN kidney of HS rats (P less than 0.05), but the 5% lower dopamine/inulin excretion from DEN than from INN of LS rats was not significant. Norepinephrine and dopamine tubular secretions from the rats, estimated by microinjecting radioactive tracers beneath the renal capsule, were 21 and 65%, respectively. After the microinjection, 68% of radioactive norepinephrine and 65% of radioactive dopamine were secreted unchanged. Catecholamine secretion rates and catabolism were not altered by denervation or different salt intakes. Estimated neural NE release was 1 ng/min in INN kidneys of both HS and LS rats; dopamine release 0.6 ng/min in kidneys of HS rats. Thus, when anesthesized, renal nerves contribute 30% to urinary NE and up to 21% to urinary dopamine excretion. Salt intake did not influence NE release from renal nerves or catecholamine secretion and catabolism by the kidney, but salt depletion decreased the renal nerve contribution to urinary dopamine excretion.
我的研究旨在测量盐摄入量对肾脏儿茶酚胺分泌和分解代谢的影响，以及肾神经对尿儿茶酚胺排泄的作用。将一侧肾脏长期去神经支配（DEN）而另一侧肾脏有神经支配（INN）的大鼠，分别给予高盐（HS）或低盐（LS）饮食5至14天。在硫喷妥钠麻醉下，用等渗盐水使大鼠扩容，而LS组大鼠给予10%甘露醇以产生相同的尿流率。LS组大鼠的肾上腺素排泄量比HS组大鼠高10倍；然而，INN肾和DEN肾的肾上腺素/菊粉排泄率相同。在HS和LS大鼠中，DEN肾的去甲肾上腺素/菊粉排泄率比INN肾低30%（P<0.01）。HS组大鼠中，DEN肾的多巴胺/菊粉排泄率比INN肾低20%（P<0.05），但LS组大鼠中DEN肾的多巴胺/菊粉排泄率比INN肾低5%，差异不显著。通过向肾被膜下微量注射放射性示踪剂估计，大鼠的去甲肾上腺素和多巴胺肾小管分泌率分别为21%和65%。微量注射后，68%的放射性去甲肾上腺素和65%的放射性多巴胺未发生变化而被分泌。去神经支配或不同的盐摄入量均未改变儿茶酚胺的分泌率和分解代谢。估计HS和LS大鼠INN肾的神经去甲肾上腺素释放量为1 ng/分钟；HS组大鼠肾脏的多巴胺释放量为0.6 ng/分钟。因此，麻醉状态下，肾神经对尿去甲肾上腺素排泄的贡献为30%，对尿多巴胺排泄的贡献高达21%。盐摄入量不影响肾神经去甲肾上腺素的释放或肾脏儿茶酚胺的分泌及分解代谢，但盐缺乏会降低肾神经对尿多巴胺排泄的贡献。
