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Renal parathyroid hormone receptors in the chick: downregulation in secondary hyperparathyroid animal models.
Am J Physiol. 1982 Mar; 242(3):E154-63.AJ

Abstract

We characterized the binding of 125I-[Nle8, Nle18, Tyr34]parathyroid hormone-(1-34) amide [125I-nlPTH-(1-34)] to renal plasma membranes prepared from chicks to determine the effects of secondary hyperparathyroid states on renal PTH receptors. This radioligand exhibited specific binding to membranes with high affinity (Kd, 2-3 X 10(-9) M). Agonists or competitive antagonists of PTH were effective in competing for binding sites labeled with 125I-nlPTH-(1-34), whereas an inactive fragment of PTH, salmon calcitonin, and bovine growth hormone did not compete with the radioligand for renal PTH receptors. Newly hatched chicks raised on control diet with adequate vitamin D and calcium or diets deficient in either vitamin D or calcium were used to study the regulation of renal PTH receptors in experimental models of secondary hyperparathyroidism. We found that both experimental diets resulted in marked hypocalcemia and progressive loss of renal cyclic AMP responsiveness to PTH in vitro. Associated with this refractoriness to the hormone was a marked reduction in PTH receptors in membranes from both vitamin D-deficient and calcium-deficient chick kidney. No change in the affinity of the PTH receptors was found. Vitamin D3, in a single dose of 250 micrograms, partially restored serum calcium of vitamin D-deficient birds toward normal by 72 h and also partly restored renal cyclic AMP responsiveness to PTH and the PTH receptor number toward control values. We conclude that renal refractoriness to PTH observed in experimentally hyperparathyroid animals models is due to a marked loss of plasma membrane receptor sites for PTH without an apparent change in the affinity of the receptors for the hormone.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

6278948

Citation

Forte, L R., et al. "Renal Parathyroid Hormone Receptors in the Chick: Downregulation in Secondary Hyperparathyroid Animal Models." The American Journal of Physiology, vol. 242, no. 3, 1982, pp. E154-63.
Forte LR, Langeluttig SG, Poelling RE, et al. Renal parathyroid hormone receptors in the chick: downregulation in secondary hyperparathyroid animal models. Am J Physiol. 1982;242(3):E154-63.
Forte, L. R., Langeluttig, S. G., Poelling, R. E., & Thomas, M. L. (1982). Renal parathyroid hormone receptors in the chick: downregulation in secondary hyperparathyroid animal models. The American Journal of Physiology, 242(3), E154-63.
Forte LR, et al. Renal Parathyroid Hormone Receptors in the Chick: Downregulation in Secondary Hyperparathyroid Animal Models. Am J Physiol. 1982;242(3):E154-63. PubMed PMID: 6278948.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal parathyroid hormone receptors in the chick: downregulation in secondary hyperparathyroid animal models. AU - Forte,L R, AU - Langeluttig,S G, AU - Poelling,R E, AU - Thomas,M L, PY - 1982/3/1/pubmed PY - 1982/3/1/medline PY - 1982/3/1/entrez SP - E154 EP - 63 JF - The American journal of physiology JO - Am. J. Physiol. VL - 242 IS - 3 N2 - We characterized the binding of 125I-[Nle8, Nle18, Tyr34]parathyroid hormone-(1-34) amide [125I-nlPTH-(1-34)] to renal plasma membranes prepared from chicks to determine the effects of secondary hyperparathyroid states on renal PTH receptors. This radioligand exhibited specific binding to membranes with high affinity (Kd, 2-3 X 10(-9) M). Agonists or competitive antagonists of PTH were effective in competing for binding sites labeled with 125I-nlPTH-(1-34), whereas an inactive fragment of PTH, salmon calcitonin, and bovine growth hormone did not compete with the radioligand for renal PTH receptors. Newly hatched chicks raised on control diet with adequate vitamin D and calcium or diets deficient in either vitamin D or calcium were used to study the regulation of renal PTH receptors in experimental models of secondary hyperparathyroidism. We found that both experimental diets resulted in marked hypocalcemia and progressive loss of renal cyclic AMP responsiveness to PTH in vitro. Associated with this refractoriness to the hormone was a marked reduction in PTH receptors in membranes from both vitamin D-deficient and calcium-deficient chick kidney. No change in the affinity of the PTH receptors was found. Vitamin D3, in a single dose of 250 micrograms, partially restored serum calcium of vitamin D-deficient birds toward normal by 72 h and also partly restored renal cyclic AMP responsiveness to PTH and the PTH receptor number toward control values. We conclude that renal refractoriness to PTH observed in experimentally hyperparathyroid animals models is due to a marked loss of plasma membrane receptor sites for PTH without an apparent change in the affinity of the receptors for the hormone. SN - 0002-9513 UR - https://www.unboundmedicine.com/medline/citation/6278948/Renal_parathyroid_hormone_receptors_in_the_chick:_downregulation_in_secondary_hyperparathyroid_animal_models_ L2 - http://journals.physiology.org/doi/full/10.1152/ajpendo.1982.242.3.E154?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -