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Protection against β adrenoceptor agonist reduction of plasma potassium in severe but not in moderate hypokalemia
Author(s) -
Tran Cao Thach,
Kjeldsen Keld
Publication year - 2011
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2011.00937.x
Subject(s) - hypokalemia , agonist , potassium , medicine , endocrinology , chemistry , receptor , organic chemistry
K‐depleted and control rats were anesthetized and infused with terbutalin. In controls, plasma K concentration (pK) decreased by 0.7 m m ( P = 0.01). In moderate hypokalemia terbutalin‐induced decrease in pK was reduced by 0.3 m m for each 1 m m decrease in pK ( n = 8, R 2 = 0.82, P = 0.002) and by 0.2 m m for each 10 mmol/g wet wt. decrease in muscle K content ( n = 8, R 2 = 0.66, P = 0.01). Hence, for baseline pK of 4, 3 and 2 m m , decrease in pK was 0.7, 0.4 and 0.1 m m , respectively. In severe hypokalemia (1.7 m m ), terbutain induced no further reduction in pK. The combined infusion of insulin and terbutalin showed no additive effect. Normalization of pK by KCl infusion in severe hypokalemia immediately abolished protection against terbutalin induced further pK reduction. Hence, terbutalin clamped pK at around 4 m m , whereas it continued to increase to around 5 m m without terbutalin infusion. Major new findings are: Protection against terbutalin induced further reduction in pK in severe pre‐existing hypokalemia (<2 m m ) and blunted but nevertheless severe further reduction in pK in more moderate pre‐existing hypokalemia; immediate abolishment of protection by normalization of pK; protection against additive reduction in pK by terbutalin and insulin in severe hypokalemia. It may be advisable to avoid hypokalemia when using β adrenoceptor agonists and to maintain pK in the upper normal range if at the risk of arrhythmia.