Eiam-ong S, Laski M E, Kurtzman N A, Sabatini S
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock 79430.
Am J Physiol. 1994 Sep;267(3 Pt 2):F390-9. doi: 10.1152/ajprenal.1994.267.3.F390.
We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.
我们研究了呼吸性酸中毒和呼吸性碱中毒对酸碱组成以及对显微解剖的肾腺苷三磷酸酶（ATP酶）的影响。将大鼠置于持续6小时、24小时和72小时的高碳酸血症或低碳酸血症环境中。高碳酸血症6小时后，集合小管（CT）的ATP酶未发生变化。24小时时，血浆碳酸氢盐为35±1毫当量/升（P<0.01），CT的H-ATP酶和H-K-ATP酶活性比对照组高90%（P<0.01）。到72小时时，血浆碳酸氢盐为37±1毫当量/升（与对照组相比P<0.005），CT酶活性进一步升高，平均约为对照组的130%（P<0.05）。在近端曲管和髓质厚升支中也观察到酶活性显著增加。在所有三个时间段，血浆醛固酮均为对照组的三到四倍。在激素充足的肾上腺切除大鼠中，酸碱参数和ATP酶活性与肾上腺完整动物所见相同。低碳酸血症6小时后，血浆碳酸氢盐无显著变化，但整个肾单位的H-ATP酶和Na-K-ATP酶活性降低了35%（P<0.05）。CT中的H-K-ATP酶活性也降低了35%。24小时时，血浆碳酸氢盐为20.5±0.5毫当量/升（与对照组相比P<0.05），CT的H-ATP酶和H-K-ATP酶活性比对照组低60%（P<0.01）。到72小时时，血浆碳酸氢盐为18.5±0.5毫当量/升（P<0.05）；然而，只有CT的H-ATP酶活性继续下降，平均比对照组低75%（P<0.005）。低碳酸血症对血浆醛固酮或钾无影响。这些结果表明，慢性而非急性呼吸性酸中毒会刺激两种肾质子ATP酶的活性。相比之下，急性和慢性呼吸性碱中毒都会降低两种肾质子泵的活性。高碳酸血症的刺激作用和低碳酸血症对肾ATP酶的抑制作用似乎与钾和醛固酮无关。尽管这些结果的确切机制尚不清楚，但可能涉及PCO2、pH或碳酸氢盐输送变化的直接作用。
