Decreased signal transduction in rat parotid cell aggregates during aging is not due to loss of alpha 1-adrenergic receptors.
Specific binding of the agonist, 3H-epinephrine, and antagonist, 3H-prazosin, to alpha 1-adrenergic receptors in both intact and broken rat parotid cell preparations was measured as a function of age in Wistar rats. Agonist binding exhibited approximately tenfold weaker affinity (Kd approximately 10 nM) for both intact and broken cells than did the antagonist (Kd approximately 1 nM). In addition, Bmax for the agonist was only 25 to 50% of that of the antagonist (7-10 fmol/mg protein vs. 15-30 fmol/mg protein) in both preparations. Binding affinity decreased significantly between ages 3 and 24 months for the antagonist but not the agonist in both intact and broken cells. The number of binding sites did not change with age in intact cells when measured with either agonist or antagonist, or when measured with agonist in broken cells, but increased markedly (approximately two fold) with age in broken cells for the antagonist. The latter results support the hypothesis that the aged rat parotid cell exhibits a naturally occurring, post-alpha 1-adrenoreceptor defect in signal transduction.
Ishikawa
Y
Y
Molecular Physiology and Genetics Section, National Institute on Aging, Francis Scott Key Medical Center, Baltimore, Maryland 21224.
Gee
M V
MV
Baum
B J
BJ
Roth
G S
GS
D000375:Aging / Q000378:metabolism*; D000818:Animals; D002449:Cell Aggregation; D002462:Cell Membrane / Q000378:metabolism; D004837:Epinephrine / Q000378:metabolism*; D008297:Male; D010306:Parotid Gland / Q000378:metabolism* / Q000648:ultrastructure; D011224:Prazosin / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D015398:Signal Transduction
D011942:Receptors, Adrenergic, alpha; D011224:Prazosin; D004837:Epinephrine