Elevation of serum potassium during beta blockade: Absence of relationship to the renin-aldosterone System

Abstract

Eighteen patients with essential hypertension were treated in a single-blind, crossover study with pindolol and with propranolol. The two drugs were compared because of known differences between them on renin secretion. We noted that plasma renin activity and plasma aldosterone concentration were suppressed by propranolol but not by pindolol. Blood pressure was reduced about equally by both drugs. Serum potassium levels rose in 17 patients on pindolol (p < 0.001) and in 14 patients on propranolol (p = 0.08). Our data suggest that serum potassium elevations induced by beta blockade do not depend on the renin-angiotensin-aldosterone system. Alternative possibilities are discussed.

Antihypertensive Therapy and Its Effects on Potassium Homeostasis

“…This process was seen with nonselective and cardioselective β blockade as well as with combined α‐β blockade 6 . The changes in serum K + concentration that accompany the administration of β blockers arise from internal K + shifts—a mechanism supported by the finding that urinary excretion of K + is not reduced when β blockade increases serum K + values 7 …”

Hyperkalemia in the elderly

“…71,72 As shown in 18 patients treated with two different ␤-adrenergic blocking medications, this effect is mediated by the blockade of ␤ 2 -adrenergic receptors, and occurs irrespective of changes in aldosterone, insulin, or glucose levels. 73 Hyperkalemia typically develops rapidly (within 24 hours), as one would expect with disruption of plasmato-tissue potassium homeostasis, but rarely develops in the absence of heavy physical activity or other risk factors for hyperkalemia. 73,74 The hyperkalemic potential of a ␤-adrenergic blocking medication is magnified by renal insufficiency, the coexistence of diabetes mellitus or hypoaldosteronism, and concurrent therapy with other medications that reduce renal potassium secretion.…”

“…73 Hyperkalemia typically develops rapidly (within 24 hours), as one would expect with disruption of plasmato-tissue potassium homeostasis, but rarely develops in the absence of heavy physical activity or other risk factors for hyperkalemia. 73,74 The hyperkalemic potential of a ␤-adrenergic blocking medication is magnified by renal insufficiency, the coexistence of diabetes mellitus or hypoaldosteronism, and concurrent therapy with other medications that reduce renal potassium secretion. [69][70][71] Heparin Hyperkalemia has been noted to occur in 7% to 8% of patients treated with at least 5,000 U of heparin twice a day.…”

Beta-Blockers, Trimethoprim-Sulfamethoxazole, and the Risk of Hyperkalemia Requiring Hospitalization in the Elderly

“…Their role in hyperkalemia through inhibition of cellular adrenergic receptor-dependent potassium translocation has been extensively studied (17)(18)(19). TMP-SMX is also in common use, representing 30% of all antibiotics prescribed for urinary tract infections (20,21).…”