The mechanism of salbutamol‐induced hypokalaemia.

Abstract

The following four intravenous treatments were administered in a balanced, randomized Latin square design to eight healthy volunteers: (‐)‐adrenaline (0.06 microgram kg‐1 min‐1 for 90 min) + vehicle control (+)‐glucose infusion (60 min), salbutamol (120 ng kg‐1 min‐1 for 30 min) + vehicle control (+)‐glucose infusion (90 min), (‐)‐adrenaline (0.06 microgram kg‐1 min‐1 for 90 min) + salbutamol (120 ng kg‐1 min‐1 for 30 min) and two vehicle control infusions of (+)‐glucose. All active solutions were preceded by a 1 h control infusion and the control infusion was continued for 1 h following the active solutions. Both the active solutions, (‐)‐adrenaline and salbutamol were increased stepwise to the above doses. Heart rate and blood pressure were recorded at frequent intervals throughout and venous blood was taken for the estimation of potassium, insulin, glucose, catecholamine and salbutamol levels. Adrenaline levels similar to those seen in acute illness were achieved using this infusion protocol. Salbutamol levels rose throughout the period of the salbutamol infusions and steady‐state was not achieved. Potassium levels were unchanged on the control + control study day and fell on all active treatments (0.45 mmol l‐1 following (‐)‐adrenaline + control; 0.48 mmol l‐1 following salbutamol + control; 0.93 mmol l‐1 following (‐)‐adrenaline + salbutamol). Insulin levels rose insignificantly after salbutamol alone and fell slightly on all other treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Salbutamol effects on systemic potassium dynamics during and following intense continuous and intermittent exercise

“…Salbutamol lowers resting plasma [K + ], whether administered intravenously (Leitch et al 1976;Whyte et al 1987;Tobin et al 2006), by ingestion (Collomp et al 2000;Edner and Jogestrand 1990;Hostrup et al 2014a;Grove et al 1995) or inhalation (Lipworth et al 1989;Bennett and Tattersfield 1997;Clark and Lipworth 1996). However, salbutamol effects on [K + ] during intense exercise remain unclear, due to previous methodological limitations.…”

Salbutamol induced hypokalaemia: the effect of theophylline alone and in combination with adrenaline.

“…Although it is fifty years since D' Silva (1934) adrenergic receptor linked to a membrane-bound found that (-)-adrenaline reduces circulating Na+/K+ ATPase pump which transfers potassium potassium concentrations it has only recently into the cells (Struthers & Reid, 1984 Hospital, Greenbank Drive, Edinburgh EH10 5SB mechanism is also the most likely explanation for the potassium lowering effect of the 12-adrenoceptor agonist, salbutamol (Whyte et al, 1987a). We have also previously demonstrated that the addition of theophylline increases (-)-adrenaline induced hypokalaemia (Whyte et al, 1987b).…”

The dose-related hyper-and-hypokalaemic effects of salbutamol and its arrhythmogenic potential

“…In some studies where hypokalaemia was reported no arrhy-' Author for correspondence. thmias were seen (Smith et al, 1984;Whyte et al, 1987;Bremner et al, 1992;Clapham & Hamilton, 1992). In another study hypokalaemia was reported after 2 h and only one subject had premature supraventricular beats (Whyte et al, 1988).…”

“…The first response was shown to be a combined a-adrenoceptor and P-adrenoceptor effect and the second response a P-adrenoceptor effect. The hypokalaemic effect of the P2-adrenoceptor agonist, salbutamol, was reported in normal volunteers within 30, 60 and 120 min of administration respectively (Smith et al, 1984;Whyte et al, 1987;1988), within 15 min in cats (Clapham & Hamilton, 1992), and within 15 min in asthmatics (Bremner et al, 1992). However, no hypokalaemia was reported in asthmatics on long-term treatment (12 months) .…”