• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肾脏氨生成对慢性呼吸性酸中毒的反应

Response of renal NH3 production to chronic respiratory acidosis.

作者信息

Rodriguez-Nichols F, Laughrey E, Tannen R L

出版信息

Am J Physiol. 1984 Dec;247(6 Pt 2):F896-903. doi: 10.1152/ajprenal.1984.247.6.F896.

DOI:10.1152/ajprenal.1984.247.6.F896
PMID:6507629
Abstract

Although chronic metabolic acidosis results in an adaptive increase in the renal capacity to produce NH3, the response to a low pH produced by chronic respiratory acidosis is unknown. Rats were placed in a specially constructed chamber with an ambient CO2 of 10% for 3 days, which increased their PCO2 to 76 +/- 4 mmHg. NH3 production was determined in vitro using both isolated kidneys perfused with 0.5 mM glutamine and cortical tubules incubated with 1 mM glutamine. Conscious rats with chronic respiratory and chronic metabolic acidosis had similar arterial pHs (7.29 +/- 0.01 and 7.31 +/- 0.01), which were significantly lower than controls (7.41 +/- 0.04). NH3 production by kidneys from rats with chronic respiratory acidosis perfused at pH 7.4 did not differ significantly from normal controls (1.13 +/- 0.13 vs. 1.07 +/- 0.17 mumol X min-1 X g-1). By contrast, kidneys from rats with chronic metabolic acidosis produced significantly more NH3 than both these groups (2.73 +/- 0.29 mumol X min-1 X g-1). Cortical tubules from rats with chronic respiratory acidosis also showed no evidence of adaptation in both NH3 (8.8 +/- 0.8 vs. 11.6 +/- 0.8 mumol X min-1 X g-1) and glucose (1.38 +/- 0.08 vs. 1.41 +/- 0.13 mumol X min-1 X g-1) production in comparison with controls, whereas chronic metabolic acidosis stimulated both ammoniagenesis and gluconeogenesis twofold or more. Thus a low systemic pH does not account for the adaptation in the capacity of the kidney to produce either ammonia or glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

尽管慢性代谢性酸中毒会导致肾脏产生NH₃的能力适应性增加,但慢性呼吸性酸中毒所产生的低pH值的反应尚不清楚。将大鼠置于一个特制的环境中,环境二氧化碳浓度为10%,持续3天,这使得它们的PCO₂升高至76±4 mmHg。使用灌注0.5 mM谷氨酰胺的离体肾脏和与1 mM谷氨酰胺一起孵育的皮质肾小管在体外测定NH₃的产生。患有慢性呼吸性和慢性代谢性酸中毒的清醒大鼠具有相似的动脉pH值(分别为7.29±0.01和7.31±0.01),显著低于对照组(7.41±0.04)。在pH 7.4灌注的慢性呼吸性酸中毒大鼠的肾脏产生的NH₃与正常对照组无显著差异(分别为1.13±0.13 vs. 1.07±0.17 μmol·min⁻¹·g⁻¹)。相比之下,慢性代谢性酸中毒大鼠的肾脏产生的NH₃明显多于这两组(2.73±0.29 μmol·min⁻¹·g⁻¹)。与对照组相比,慢性呼吸性酸中毒大鼠的皮质肾小管在NH₃(分别为8.8±0.8 vs. 11.6±0.8 μmol·min⁻¹·g⁻¹)和葡萄糖(分别为1.38±0.08 vs. 1.41±0.13 μmol·min⁻¹·g⁻¹)产生方面也没有适应的迹象,而慢性代谢性酸中毒使氨生成和糖异生增加了两倍或更多。因此,全身低pH值并不能解释肾脏产生氨或葡萄糖能力的适应性变化。(摘要截取自250字)

相似文献

1
Response of renal NH3 production to chronic respiratory acidosis.肾脏氨生成对慢性呼吸性酸中毒的反应
Am J Physiol. 1984 Dec;247(6 Pt 2):F896-903. doi: 10.1152/ajprenal.1984.247.6.F896.
2
Stimulation of ammoniagenesis by acute acidosis: evidence for a urinary inhibitor.急性酸中毒对氨生成的刺激作用:关于一种尿中抑制剂的证据。
Am J Physiol. 1980 Nov;239(5):F445-51. doi: 10.1152/ajprenal.1980.239.5.F445.
3
Influence of phosphoenolpyruvate carboxykinase inhibition on the response of NH3 production to acute acidosis.磷酸烯醇式丙酮酸羧激酶抑制对氨生成对急性酸中毒反应的影响。
J Lab Clin Med. 1983 Aug;102(2):198-204.
4
Response of ammoniagenesis to acute alkalosis.
Am J Physiol. 1984 Nov;247(5 Pt 2):F827-36. doi: 10.1152/ajprenal.1984.247.5.F827.
5
Urinary inhibitor of the ammoniagenic response to acute acidosis is a prostaglandin.急性酸中毒产氨反应的尿抑制物是一种前列腺素。
J Lab Clin Med. 1986 Oct;108(4):277-85.
6
Effect of respiratory acidosis on intracellular pH of the proximal tubule.
Am J Physiol. 1986 Jun;250(6 Pt 2):F1039-45. doi: 10.1152/ajprenal.1986.250.6.F1039.
7
Absence of adaptation in renal NH3 production to chronic respiratory acidosis.肾脏氨生成对慢性呼吸性酸中毒缺乏适应性。
Contrib Nephrol. 1985;47:64-9. doi: 10.1159/000411210.
8
Adaptive changes in renal acidification in response to chronic respiratory acidosis.慢性呼吸性酸中毒时肾脏酸化功能的适应性变化。
Am J Physiol. 1985 Apr;248(4 Pt 2):F492-9. doi: 10.1152/ajprenal.1985.248.4.F492.
9
The impact of acetazolamide on renal ammoniagenesis and gluconeogenesis.
J Lab Clin Med. 1983 Oct;102(4):536-42.
10
Ammonia production by isolated mouse proximal tubules perfused in vitro. Effect of metabolic acidosis.体外灌注的分离小鼠近端小管的氨生成。代谢性酸中毒的影响。
J Clin Invest. 1986 Jul;78(1):124-9. doi: 10.1172/JCI112540.

引用本文的文献

1
Differential effects of deleting the angiotensin receptor AT on the whole animal response to respiratory and metabolic acidosis in mice.删除血管紧张素受体AT对小鼠对呼吸性和代谢性酸中毒的整体动物反应的不同影响。
Am J Physiol Regul Integr Comp Physiol. 2025 Sep 1;329(3):R441-R458. doi: 10.1152/ajpregu.00088.2025. Epub 2025 Jul 18.
2
Effects of chronic hypercapnia on ammonium transport in the mouse kidney.慢性高碳酸血症对小鼠肾脏铵转运的影响。
Physiol Rep. 2019 Aug;7(16):e14221. doi: 10.14814/phy2.14221.
3
Secondary Response to Chronic Respiratory Acidosis in Humans: A Prospective Study.
人类慢性呼吸性酸中毒的继发性反应:一项前瞻性研究。
Kidney Int Rep. 2018 Jun 8;3(5):1163-1170. doi: 10.1016/j.ekir.2018.06.001. eCollection 2018 Sep.
4
Hypokalemic nephropathy in the rat. Role of ammonia in chronic tubular injury.大鼠低钾血症性肾病。氨在慢性肾小管损伤中的作用。
J Clin Invest. 1987 May;79(5):1447-58. doi: 10.1172/JCI112973.
5
Induction of hypertrophy in cultured proximal tubule cells by extracellular NH4Cl.细胞外氯化铵诱导培养的近端小管细胞肥大。
J Clin Invest. 1989 Dec;84(6):1767-79. doi: 10.1172/JCI114361.