Open AccessThe Influence of Chronic Hypokalemia on Myocardial Adrenergic Receptor Densities
Author(s) -
David J. Miletich,
Richard D. Minshall,
Ronald F. Albrecht
Publication year - 1997
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1097/00000539-199704000-00006
Subject(s) - prazosin , medicine , hypokalemia , epinephrine , propranolol , endocrinology , adrenergic receptor , receptor , alpha (finance) , adrenergic , antagonist , surgery , construct validity , patient satisfaction
We studied the effects of a 30-day potassium (K+)-deficient diet on blood [K+] myocardial adrenergic receptor densities, serum catecholamines, and epinephrine arrhythmogenicity in adult laboratory rats (250 +/- 25 g). Within 3 days of beginning the K+-deficient diet, blood [K+] decreased by 50%. After 5 days, the myocardial alpha-1 density increased (62 +/- 2 vs 148 +/- 16 fmols/mg protein), and the total beta receptor increased (95 +/- 5 vs 273 +/- 49) without significant change in receptor affinity. However, 18-21 days of this diet was necessary to produce an increase in the duration of epinephrine arrhythmias (from 56 +/- 8 to 224 +/- 21 s). While prazosin block of the alpha-1 receptor in hypokalemic rats caused a significant, 42% reduction in arrhythmic duration and propranolol block caused a 62% reduction, both prazosin and propranolol were necessary to return arrhythmia times to normal (44 +/- 0.3 mmols/dL). Total serum catecholamines were reduced after 3 days of the diet (from 482 +/- 37 to 299 +/- 31 pg/ml) and remained depressed throughout the 30 days of the K+ diet. The results of this study indicate that prolonged restriction causes a reduction in serum catecholamines, an increase in myocardial alpha-1 and beta receptors densities, and an increase in epinephrine arrhythmogenicity. All of these changes were reversed within 5 days of initiating a normal dietary K+ intake.