Membrane proteins of the myocytes in cardiac overload.
Hypertrophy of the cardiac myocytes resulting from a mechanical overload may be responsible for major membraneous modifications, either at a sarcolemmal or at a sarcoplasmic level. In the present report, evaluation of several sarcolemmal markers such as beta-receptors, muscarinic receptors or (Na+,K+)-ATPase has been realized on an experimental model of cardiac hypertrophy performed on adult rats. Special attention has been taken to compare results expressed in densities or expressed in number of receptors present at the cellular level. For example, the beta-receptors density was 30% decreased whereas calculations of number of receptors present in the myocytes revealed an unchanged number (around 20,000 in both groups). The unmodified number could suggest a non regulation for the genes coding for the receptors.
Mansier
P
P
Hôpital Lariboisière, Unité Inserm 127, Paris, France.
Chevalier
B
B
Mayoux
E
E
Charlemagne
D
D
Ollivier
L
L
Callens-el Amrani
F
F
Swynghedauw
B
B
D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000032:analysis*; D051381:Rats; D011919:Rats, Inbred Strains; D011943:Receptors, Adrenergic, beta / Q000032:analysis*; D011976:Receptors, Muscarinic / Q000032:analysis*; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis*
D008565:Membrane Proteins; D011943:Receptors, Adrenergic, beta; D011976:Receptors, Muscarinic; D000254:Sodium-Potassium-Exchanging ATPase