Endocrinological aspects of PTH metabolism in the kidney.
Various methods for the measurement of intact PTH, PTH fragments and PTH binding to receptors were applied to clarify the role of renal receptors for the bioexpression of PTH. Glomerular receptors may contribute approximately 20% of the renal PTH catabolism. PTH also binds to tubular receptors at the luminal side (brush border membranes) as well as at the antiluminal site (basal-lateral membrane). Scatchard plot analysis of PTH binding to these receptors allows the calculation of an equilibrium dissociation constant and binding capacity, if correction is made for inactivation of bioactive PTH (measured by LAMA). Binding to receptors is--in our systems--invariably associated with degradation of the intact hormone to N-terminal and C-terminal fragments of different molecular weight. Antibodies against basal lateral membranes and against brush border membranes are able to inhibit PTH binding to tubular membranes. Sera of uremic patients with inappropriately high PTH contain a globulin which interferes with PTH binding to the receptor, suggesting that uremia may be another example for a "hormone receptor antibody disease".
D000818:Animals; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism; D007700:Kinetics; D008871:Microvilli / Q000187:drug effects / Q000378:metabolism; D008970:Molecular Weight; D010281:Parathyroid Hormone / Q000378:metabolism* / Q000494:pharmacology; D011956:Receptors, Cell Surface / Q000378:metabolism; D013329:Structure-Activity Relationship; D014511:Uremia / Q000503:physiopathology
D010281:Parathyroid Hormone; D011956:Receptors, Cell Surface