title: Effects of lovastatin treatment on red blood cell and platelet cation transport.
abstract: Hypercholesterolemia frequently accompanies hypertension, and it has been suggested that by affecting membrane lipid composition, hypercholesterolemia may cause or accentuate abnormalities in several red blood cell transports associated with hypertension. Such an effect might obfuscate the relation of membrane markers to hypertension and decrease their usefulness in genetic studies of the heritable basis of hypertension. To determine if changing plasma lipids affects membrane transport, we studied the effects of the cholesterol-lowering agent lovastatin on red blood cell lithium-sodium countertransport and sodium-potassium-chloride cotransport, red blood cell sodium and water content, and platelet amiloride-sensitive volume responsiveness to cytoplasmic acidification, an indirect measure of sodium-proton exchange that has been proposed as a new membrane marker for hypertension. In a 24-week, placebo-controlled, double-blinded, randomized trial, lovastatin significantly lowered total and low density lipoprotein cholesterol and raised high density lipoprotein cholesterol. Red blood cell lithium-sodium countertransport and sodium-potassium-chloride cotransport were not significantly altered. Red blood cell sodium content decreased significantly in the lovastatin-treated group, probably as a result of an increase in red blood cell sodium-potassium pump activity. Platelet amiloride-sensitive responses to cytoplasmic acidification were significantly depressed by lovastatin treatment, suggesting that lowering plasma cholesterol may suppress platelet sodium-proton exchange. It has been hypothesized that the hyperlipidemias frequently observed in essential hypertensive patients may alter membrane lipid composition and affect membrane cation transport activities.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: University of Michigan Medical Center, Department of Internal Medicine, Ann Arbor 48109-0356.
authors.forename: A B
authors.initials: AB
authors.lastname: Weder
authors.forename: C
authors.initials: C
authors.lastname: Serr
authors.forename: B A
authors.initials: BA
authors.lastname: Torretti
authors.forename: D R
authors.initials: DR
authors.lastname: Bassett
authors.forename: A J
authors.initials: AJ
authors.lastname: Zweifler
mesh_terms: D000704:Analysis of Variance; D017920:Antiporters; D001692:Biological Transport; D001792:Blood Platelets / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D002412:Cations / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008148:Lovastatin / Q000494:pharmacology*; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D008875:Middle Aged; D011422:Propionates / Q000494:pharmacology; D028021:Sodium-Potassium-Chloride Symporters
chemical_list: D017920:Antiporters; D002352:Carrier Proteins; D002412:Cations; D008055:Lipids; D008565:Membrane Proteins; D011422:Propionates; D028021:Sodium-Potassium-Chloride Symporters; C045885:sodium-lithium countertransporter; D008148:Lovastatin; C029658:propionic acid