Anderson R J, Henrich W L, Gross P A, Dillingham M A
Circ Res. 1982 Feb;50(2):294-300. doi: 10.1161/01.res.50.2.294.
Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. We, therefore, increased PCO2 from 23 to 74 mm Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 muEq/min, P less than 0.001) and fractional excretion of sodium (4.0 to 1.2 %, P less than 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, PO2, glomerular filtration rate, renal blood flow, extraction of P-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of 1-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal alpha-adrenergic nerves and the renal angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.
尽管临床研究表明慢性高碳酸血症性酸中毒可能与肾钠潴留有关，但关于急性高碳酸血症性酸中毒对肾钠排泄的影响却知之甚少。因此，我们将麻醉犬的PCO₂从23mmHg提高到74mmHg，观察到明显的钠排泄减少，绝对钠排泄量（从235降至60μEq/min，P<0.001）和钠分数排泄率（从4.0%降至1.2%，P<0.02）均显著降低。钠排泄的减少与肾灌注压、PO₂、肾小球滤过率、肾血流量、对氨基马尿酸提取率及滤过分数的持续变化无关。急性高碳酸血症性酸中毒引起的钠排泄减少反应可通过手术去肾神经、肾内注射酚苄明以及肾内输注1-肌氨酸,8-甘氨酸血管紧张素II而显著减弱。给予10mg/kg消炎痛可增强去神经肾对高碳酸血症性酸中毒的钠排泄减少反应。这些结果提示，肾α-肾上腺素能神经和肾血管紧张素系统在急性高碳酸血症性酸中毒时导致钠排泄减少效应。肾前列腺素或相关物质可能起到减弱这种钠排泄减少反应的作用。
