Stemmer C L, Perez G O, Oster J R
Medical Service, Veterans Administration Medical Center, Miami, FL 33125.
J Clin Pharmacol. 1987 Aug;27(8):628-31. doi: 10.1002/j.1552-4604.1987.tb03077.x.
An abnormality of extrarenal mechanisms is believed to contribute importantly to the impaired potassium homeostasis in chronic renal failure. We evaluated the plasma potassium response to inhalation of albuterol, a beta 2 agonist, in eight patients who had end-stage renal disease and who were undergoing chronic hemodialysis and in eight control subjects. The purpose was to assess if an abnormality of the beta 2 adrenoceptor mechanism is present in uremia. The maximal decrement in plasma potassium concentration in the patients (0.12 +/- 0.04 mEq/L) was significantly less than that of the control subjects (0.30 +/- 0.05). Furthermore, the final plasma potassium concentration slightly exceeded baseline in the patients but was significantly reduced in controls, leading to the conclusion that an abnormal responsiveness of the beta 2 adrenoceptor may contribute to the impaired potassium tolerance found in patients who have end-stage renal disease.
肾外机制异常被认为在慢性肾衰竭患者钾稳态受损中起重要作用。我们评估了8例终末期肾病且正在接受慢性血液透析的患者及8例对照者吸入β2激动剂沙丁胺醇后血浆钾的反应。目的是评估尿毒症患者是否存在β2肾上腺素能受体机制异常。患者血浆钾浓度的最大降幅（0.12±0.04 mEq/L）显著低于对照者（0.30±0.05）。此外，患者最终血浆钾浓度略超过基线水平，而对照者则显著降低，由此得出结论，β2肾上腺素能受体反应异常可能导致终末期肾病患者钾耐受性受损。
