Effects of parathyroid hormone on renal tubular reabsorption of calcium, sodium, and phosphate

Agus, Z. S.; Gardner, LB; Lh, Beck; M, Goldberg

doi:10.1152/ajplegacy.1973.224.5.1143

Cited by 288 publications

(123 citation statements)

References 0 publications

Supporting

Mentioning

115

Contrasting

Unclassified

Order By: Relevance

“…To help resolve this conflict we studied the effects of a purified PTE, that is devoid of hemodynamic effects (31,32), in intact and TPTX dogs loaded with bicarbonate. The infusion of PTE in a dose similar to that previously employed by Hellman et al (10) led to a fall in bicarbonate absorption in both groups, but more marked in the TPTX group.…”

Section: Discussionmentioning

confidence: 99%

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

et al. 1974

View full text Add to dashboard Cite

A B S T R A C T The role of parathyroid hormone (PTH) and of Ca++ in the regulation of bicarbonate absorption (RHCO3) and its response to extracellular volume expansion (VE) was studied in HC03-loaded dogs.VE lowered RHCO3 in both intact (from 24.8 to 22.0 mmol/liter GFR, P < 0.01) and thyroparathyroidectomized (TPTX) (from 24.5 to 18.0 mmol/liter GFR, P < 0.001) dogs; glomerular filtration rate (GFR) and filtered HCOi-did not change. Both groups showed a significant increase in the fractional excretion of sodium (CNa X 100/GFR), calcium (CCa X 100/ GFR), and chloride (Cci X 100/GFR) and a decrease in phosphorus reabsorption. Fractional clearance of phosphate (CP X 100/GFR) rose in both groups but did not achieve significance.Infusion of purified parathyroid extract (PTE) decreased RHCOs in intact dogs (from 24.6 to 22.5 mmol/ liter GFR, P < 0.025) and in TPTX dogs (from 26.9 to 22.6 mmol/liter GFR, P < 0.05). No Infusion of Ca++ raised ultrafilterable Ca++ from 5.7 to 7.9 mg/100 ml in intact and from 4.9 to 7.2 mg/ 100 ml in TPTX dogs; RHCOs increased in intact (from 22.9 to 26.9 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.6 to 28.6 mmol/liter GFR, P <0.05). The GFR, RBF, and the fractional excretion of sodium, chloride, and calcium did not change in either group. The reabsorbed phosphate increased in both groups, and fractional phosphorus clearance fell in the intact group but did not change significantly in the TPTX group.Superimposition of PTE on hypercalcemia in TPTX dogs resulted in a decrease in RHco8 (from 27.3 to 23.9 mmol/liter GFR, P < 0.001), which was accompanied by an increase in the fractional excretion of phosphate and a decrease in the reabsorbed phosphate. In this group of TPTX dogs hypercalcemia caused a drop in RBF from 135.6 to 105.8 ml/min with no change in GFR. The RBF returned to control value with PTE infusion.It is concluded that: (a) the lowering of RHCO3 by VE is not dependent solely on stimulation of PTH by the lowered Ca', (b) PTE acts directly on the renal tubules to lower RHCOs, (c) Ca' enhances RHcos and this effect is exerted in the absence of PTH and calcitonin, (d) neither the effects of CaZ nor of PTH appear to be mediated by altered hemodynamics, although this cannot be excluded in Ca^-infused TPTX dogs, (e) Ca' enhanced phosphate reabsorption in the absence of PTH; this may be a specific effect of hypercalcemia on phosphate reabsorption or the nonspecific consequence of the rise in serum phosphorus.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

et al. 1974

View full text Add to dashboard Cite

show abstract

“…1) and this suggests that there may have been an inhibition ofPTH secretion but other undefined factors which can increase fractional phosphate excretion independently of PTH may have been involved (Swenson et al 1975). Certainly the diminution of calcium clearances prior to the attainment of the peak sodium or phosphate clearances is consistent with PTH intervention (Agus et al 1973) but this effect also may arise by different mechanisms (Hulley et al 1969). Although several workers have shown a direct relationship between phosphate and sodium reabsorption by the renal tubule (see Knox et al 1973), the relationship seen here could be expected in that both sodium and phosphate are simultaneously infused.…”

Section: Excretion Of Cationsmentioning

confidence: 98%

Renal Response to Intravenous Phosphate Infusion in the Sheep

Fürst¹

1975

Aust. Jnl. Of Bio. Sci.

View full text Add to dashboard Cite

Renal clearance experiments were performed on six Merino ewes in which plasma phosphate concentrations were increased by the intravenous infusion of isohydric sodium phosphate. As the phosphate load to the kidney increased, the renal tubular reabsorptive capacity became saturated and a definite tubular maximum for phosphate reabsorption (Tmp) was demonstrated. The Tmp was directly related to the glomerular filtration rate and had a mean value of 333·1 ± 27·0 (S.E.M.) /lmol! min or 416· 6± 13· 5/lmol!100 ml glomerular filtrate. Calcium infused concurrently with phosphate in order to maintain plasma total calcium levels did not alter the Tmp. Ultrafilterability of calcium and phosphate in the plasma decreased with phosphate infusion and this was accentuated by an accompanying calcium infusion.The Tmp in sheep's kidney is higher than in non-ruminant animals and the implications of this are discussed.

show abstract

“…Decades of research have established PTH as a major systemic hormone that controls mineral ion homeostasis and bone maintenance (4,5). In response to either low calcium or high phosphate levels in the circulation, PTH is synthesized and secreted into the bloodstream as an 84-amino acid polypeptide from the chief cells of the parathyroid glands (6,7).…”

mentioning

confidence: 99%

Molecular recognition of parathyroid hormone by its G protein-coupled receptor

Pioszak

2008

Proc. Natl. Acad. Sci. U.S.A.

238

313

View full text Add to dashboard Cite

Parathyroid hormone (PTH) is central to calcium homeostasis and bone maintenance in vertebrates, and as such it has been used for treating osteoporosis. It acts primarily by binding to its receptor, PTH1R, a member of the class B G protein-coupled receptor (GPCR) family that also includes receptors for glucagon, calcitonin, and other therapeutically important peptide hormones. Despite considerable interest and much research, determining the structure of the receptor-hormone complex has been hindered by difficulties in purifying the receptor and obtaining diffraction-quality crystals. Here, we present a method for expression and purification of the extracellular domain (ECD) of human PTH1R engineered as a maltose-binding protein (MBP) fusion that readily crystallizes. The 1.95-Å structure of PTH bound to the MBP-PTH1R-ECD fusion reveals that PTH docks as an amphipathic helix into a central hydrophobic groove formed by a three-layer ␣-␤-␤␣ fold of the PTH1R ECD, resembling a hot dog in a bun. Conservation in the ECD scaffold and the helical structure of peptide hormones emphasizes this hot dog model as a general mechanism of hormone recognition common to class B GPCRs. Our findings reveal critical insights into PTH actions and provide a rational template for drug design that targets this hormone signaling pathway.calcitonin ͉ crystal structure ͉ glucagon ͉ maltose-binding protein ͉ osteoporosis

show abstract

Effects of parathyroid hormone on renal tubular reabsorption of calcium, sodium, and phosphate

Cited by 288 publications

References 0 publications

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

Renal Response to Intravenous Phosphate Infusion in the Sheep

Molecular recognition of parathyroid hormone by its G protein-coupled receptor

Contact Info

Product

Resources

About