title: Adrenergic modulation of extrarenal potassium disposal in men with end-stage renal disease.
abstract: In normal subjects, beta-adrenergic stimulation lowers the serum potassium, whereas alpha-stimulation raises it. Epinephrine, a mixed alpha and beta agonist, acutely lowers the blood potassium in normal subjects, but not in patients with end-stage renal disease. This study was designed to determine whether the resistance to the hypokalemic effect of epinephrine in dialysis patients is due to a blunted beta-adrenergic response, or to an augmented alpha-adrenergic response. The infusion of epinephrine at low doses (0.01 microgram/kg/min) produced a significant increase in serum potassium in hemodialysis patients (+0.21 +/- 0.07 mmol/liter, P less than 0.05), as compared to a nonsignificant decrease (-0.06 +/- 0.04 mmol/liter) in normal subjects. Epinephrine at high physiologic doses (0.04 microgram/kg/min) failed to significantly change the serum potassium in the dialysis patients (-0.10 +/- 0.14 mmol/liter), but substantially lowered serum potassium in the controls (-0.64 +/- 0.10 mmol/liter, P less than 0.001). There was no significant correlation (r = 0.03) between the baseline serum potassium concentration and the magnitude of change during epinephrine infusion. Epinephrine infusion (0.04 microgram/kg/min) during beta-blockade with propranolol produced a greater rise in serum potassium in the dialysis patients as compared to the controls (+0.69 +/- 0.11 vs. +0.32 +/- 0.11 mmol/liter, P less than 0.05). Epinephrine infusion (0.01 microgram/kg/min) during alpha-blockade with phentolamine resulted in similar changes in serum potassium in dialysis patients and in normal control (-0.10 +/- 0.12 vs. -0.10 +/- 0.06 mmol/liter). Moreover, phentolamine reversed the increase in serum potassium observed in dialysis patients during the infusion of epinephrine following beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Nephrology Research and Training Center, University of Alabama, Birmingham.
authors.forename: M
authors.initials: M
authors.lastname: Allon
authors.forename: N
authors.initials: N
authors.lastname: Shanklin
mesh_terms: D000328:Adult; D004837:Epinephrine / Q000494:pharmacology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010646:Phentolamine / Q000494:pharmacology; D011188:Potassium / Q000097:blood*; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism; D006435:Renal Dialysis
chemical_list: D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D011433:Propranolol; D011188:Potassium; D004837:Epinephrine; D010646:Phentolamine