Na,K-pump concentration in hypertrophied human hearts.
Several studies have associated myocardial dysfunction with reduced myocardial Na,K-pump concentration, but whether impaired Na,K-pump capacity is a pathogenetic factor or an epiphenomenon related to accompanying cardiac hypertrophy is not established. We measured Na,K-pump concentrations in 10 hypertrophied and 11 normal weighted hearts obtained at autopsy using [3H]ouabain as ligand. Specific [3H] ouabain binding site concentration (OBC) in the left ventricle (LV) averaged 449 +/- 40 (pmol.g-1 wet weight; mean +/- SEM) in hypertrophied and 598 +/- 36 in normal weighted ventricles (P = 0.02). A trend towards lower LV OBC (-19%; P = 0.25) was found in hypertrophied hearts from patients with congestive heart failure as compared with non-failing hypertrophied hearts. In multivariate analysis with 18 variables including age and heart failure, only LV weight correlated independently with LV OBC (r = -0.61; P = 0.003). When OBC was related to either dry weight or to protein content, a 25-35% reduction was consistently found in hypertrophied LV, whereas RV OBC was similar in both groups. In conclusion, myocardial Na,K-pump concentration and thus the capacity to maintain homeostasis is reduced in LV, but not in RV, of hypertrophied hearts. Whether the moderately reduced myocardial Na,K-pump concentration is a pathogenetic factor in LV dysfunction remains to be determined.
Ellingsen
O
O
Department of Cardiology, University of Oslo, Ullevål Hospital, Norway.
Holthe
M R
MR
Svindland
A
A
Aksnes
G
G
Sejersted
O M
OM
Ilebekk
A
A
D000368:Aged; D001824:Body Constitution; D006332:Cardiomegaly / Q000378:metabolism*; D006333:Heart Failure / Q000378:metabolism; D006352:Heart Ventricles / Q000737:chemistry; D006801:Humans; D009206:Myocardium / Q000737:chemistry; D010042:Ouabain / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis*
D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase