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Impairment of β 2 ‐Adrenoceptor‐Stimulated Potassium Uptake in End‐Stage Renal Disease
Author(s) -
Stemmer Craig L.,
Perez Guido O.,
Oster James R.
Publication year - 1987
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1987.tb03077.x
Subject(s) - medicine , potassium , uremia , hemodialysis , endocrinology , end stage renal disease , abnormality , agonist , homeostasis , hyperkalemia , kidney disease , chemistry , receptor , organic chemistry , psychiatry
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 β 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 β 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 β 2 adrenoceptor may contribute to the impaired potassium tolerance found in patients who have end‐stage renal disease.