The effect of intravenously administered salbutamol on serum potassium in asthmatic and nonasthmatic atopic subjects

Abstract

The role of adrenergic mechanism in the pathogenesis of allergic disease is controversial. Recent experimental and clinical reports have suggested that beta-adrenergic blockade impairs and beta stimulation enhances extrarenal potassium uptake in humans. This led us to study the effect of the intravenous administration of salbutamol, a specific beta-2-adrenergic agonist, on serum potassium in 9 healthy subjects and in 23 patients with allergic asthma and/or rhinitis. Serum potassium fell significantly and reached a peak decline at the end of venous infusion in all the normal subjects. Seventeen atopic subjects showed a lower or absent serum K+ decrement: there was no difference between asthmatic and rhinitic patients. There was no relation among the salbutamol-induced serum potassium decrement, serum glucose increment, blood pressure and heart-rate changes, and nonspecific bronchial reactivity. These findings suggest that beta-2-adrenergic hyporesponsiveness is present only in some allergic patients.

Decrease of plasma potassium due to inhalation of beta‐2‐agonists: absence of an additional effect of intravenous theophylline

“…Beta-2-agonists and theophylline have an additive bronchodilating effect on reactive airways and for this reason are often used in combination in COPD patients. The intravenous, oral or subcutaneous administration of beta-Z-agonists causes a decrease of plasma potassium [6][7][8][9][10]. In the present study in volunteers this also occurred after inhalation of salbutamol and terbutaline, as we showed earlier for fenoterol [1].…”

The Wiser Strategy of Using Beta-Agonists in Asthma: Mechanisms and Rationales

“…Intravenous beta-agonist administration can induce serious outcomes such as hypokalemia, demanding vigilant monitoring, while high doses may lead to lactic acidosis. 30 31 Therefore, caution is advised, especially in patients with conditions such as ischemic heart disease, hyperthyroidism, and diabetes, all of which can worsen by excessive beta-agonist use. Cardiac side effects, which have been previously implicated in increased asthma mortality, 32 can be more dangerous under hypoxemic conditions.…”

High Proximal Excretion of Sodium during Activation of β₂-Adrenoreceptors in Humans

“…The effects of |}2-type adrenoreceptors on electrolyte homeostasis are sec ondary to both transport across cell membrane as well as renal mechanisms and mediated at least in part by a tend ency towards high circulating insulin and renin [1][2][3][4][5][6][7]. Data on the influence of p2-type adrenoreceptors on renal hand ling of sodium are scanty.…”