Renal handling of calcium: influence of parathyroid hormone and 1,25-dihydroxyvitamin D3

1979 ◽  
Vol 236 (4) ◽  
pp. F349-F356 ◽  
Author(s):  
K. Hugi ◽  
J. P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Plasma Concentration ◽  
Normal Level ◽  
Linear Increase ◽  
Renal Handling ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Intestinal Ca Absorption ◽  
Filtered Load

The influence of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on the renal Ca handling was studied in vitamin D-replete rats. The relation between plasma concentration ([Ca]P) and urinary Ca (UCaV/ml GF) was ascertained by clearance techniques over the [Ca]P range of 1.4-3.4 mM varied by infusion of Ca gluconate. Chronic thyroparathyroidectomy (TPTX) decreased the plasma Ca threshold from about 2.3 to 1.5 mM. Between [Ca]P 1.4 and 3.4 mM there was a linear increase in UCaV/ml GF corresponding to 35-50% of the increment in filtered load. In TPTX, PTH (2.5 IU/h i.v.) shifted the Ca threshold from 1.5 to 2.3 mM, without changing the slope of UCaV/ml GF on [Ca]P. The effect of TPTX on the renal Ca handling was not corrected by doses of 1,25(OH)2D3, which increased the intestinal Ca absorption of TPTX rats to normal level. In intact and TPTX rats disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) given at doses which inhibit the production of 1,25(OH)2D3 did not change the tubular Ca handling. Furthermore, 1,25(OH)2D3 had no effect in EHDP-treated TPTX rats. Therefore, tubular Ca handling does not appear to be altered in response to chronic endogenous variation or physiologic supplementation of 1,25(OH)2D3 in vitamin D-replete rats. This is in contrast to the marked alteration observed after TPTX or PTH administration.

Insulin modulates the stimulation of renal 1,25-dihydroxyvitamin D3 production by parathyroid hormone

1985 ◽  
Vol 109 (2) ◽  
pp. 243-248 ◽  
Author(s):  
Nirandon Wongsurawat ◽  
H. James Armbrecht
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Diabetic Rats ◽  
Biologically Active ◽  
Renal Handling ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
Maximal Stimulation ◽  
Insulin Replacement ◽  
Stimulation Of

Abstract. Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 ± 2 vs 46 ± 5 pg/min/g; P < 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 ± 1 vs 19 ± 4 pg/min/g; P < 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 ± 12 vs 19 ± 4 pg/min/g; P < 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.

Independence of salt intake from the hormones regulating calcium homeostasis

1993 ◽  
Vol 264 (3) ◽  
pp. R500-R512 ◽  
Author(s):  
M. G. Tordoff ◽  
R. L. Hughes ◽  
D. M. Pilchak
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Calcium Homeostasis ◽  
Salt Intake ◽  
Calcium Content ◽  
Deficient Diet ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Chronic Infusion ◽  
Intact Rats

Rats deprived of dietary calcium increase voluntary intake of NaCl solutions. We investigated whether the major hormones controlling calcium homeostasis are responsible for this increase in salt intake. Removing endogenous sources of calcitonin and parathyroid hormone by thyroidectomy and/or parathyroidectomy had no effect on NaCl intake. The surgically compromised rats and their intact controls drank similar amounts of NaCl in response to manipulations of diet calcium content. Despite normal NaCl intakes, rats with parathyroidectomy had low plasma calcium concentrations and a strong appetite for 50 mM CaCl2 solution. Chronic infusion of parathyroid hormone into rats with thyroparathyroidectomy decreased NaCl intake. Intact rats fed an American Institute of Nutrition (AIN)-76A-based vitamin D-deficient diet increased NaCl intake slightly and showed a strong appetite for CaCl2, but other rats maintained normocalcemic by the addition of calcium, phosphorus, and lactose to the vitamin D-deficient diet had normal NaCl and CaCl2 intakes. Chronic infusions of 1,25-dihydroxyvitamin D3 into intact rats had no effect on NaCl intake. Taken together, these results indicate that the increase in NaCl intake produced by calcium deprivation is not mediated by changes in circulating levels of calcium, calcitonin, parathyroid hormone, or 1,25-dihydroxyvitamin D3. Furthermore, the major calcium-regulating hormones are not involved in the control of "spontaneous" NaCl intake in the rat.

Effect of vitamin D sterols and dietary magnesium on calcium and phosphorous homeostasis

1981 ◽  
Vol 241 (1) ◽  
pp. E35-E41 ◽  
Author(s):  
B. S. Levine ◽  
M. W. Walling ◽  
J. W. Coburn
Keyword(s):  
Vitamin D ◽  
Bone Resorption ◽  
Vitamin D3 ◽  
The Other ◽  
Vitamin D Status ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Dietary Magnesium ◽  
Intestinal Ca Absorption ◽  
P Absorption

Calcium (Ca) and phosphorus (P) metabolism were studied in vitamin D-deficient rats as vitamin D status and dietary magnesium (Mg) were varied. Rats given normal (0.03%) or high (0.2%) Mg diets received either vehicle, vitamin D3 (1,650 pmol/day), or 1,25-dihydroxyvitamin D3 (60 pmol/day) for 9 days. In vitamin D-deficient rats, high dietary Mg lowered intestinal Ca absorption from 40 +/- 5 to 11 +/- 5%; P absorption decreased 50%. Treatment with 1,25-dihydroxyvitamin D3 prevented the Mg-induced fall in absorption; vitamin D3 did so only for the first 6 days. The total Ca and Mg (Ca + Mg) absorbed (mM/day) decreased from 0.85 +/- 0.050 mM/day to 0.14 +/- 0.10 with the high dietary Mg; 1,25-dihydroxyvitamin D3 treatment raised Ca + Mg absorption regardless of diet Mg; high dietary Mg raised serum Ca despite a decreased intestinal Ca absorption and urinary Ca; treatment with either sterol had no added calcemic effect. These results are consistent with two processes for intestinal Ca and P transport: one vitamin D-dependent and the other non-vitsamin D-dependent and inhibited by high dietary Mg. Also high dietary Mg increases serum Ca, perhaps by affecting bone resorption.

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