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PubMed1980

Calcium-dependent, parathyroid hormone-independent regulation of 1,25-dihydroxyvitamin D.

The increase of plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) in response to Ca restriction has been suggested to be essentially mediated by parathyroid hormone (PTH). In this study, we have assessed the influence of variations in calcium intake on plasma 1,25(OH)2D in pair-fed sham-operated (sham) and in hypocalcemic hypoparathyroid rats after thyroparathyroidectomy (TPTX). In sham rats, plasma 1,25(OH)2D increased from 189 +/- 16 to 486 +/- 41 pM when dietary calcium was inreased from 1.2% Ca to 0.2% Ca. This increase was associated with an increase in plasma PTH level. In TPTX rats, plasma 1,25(OH)2D increased from 112 +/- 9 to 332 +/- 36 pM when dietary calcium was decreased. In this case, the increase was not associated with a rise in plasma PTH level nor with an increase in urinary cyclic AMP. When TPTX rats were infused chronically with PTH (60 U/day), plasma 1,25(OH)2D was 62 +/- 9 pM when the 1.2% Ca diet was given and 281 +/- 45 pM with the 0.2% Ca diet. These reults confirm that the thyroparathyroid glands influence plasma 1,25(OH)2D but they also provide evidence for a PTH-independent response of plasma 1,25(OH)2D to Ca restriction.

Animals↗

PubMed1980

Regulation of renal adenylate cyclase by parathyroid hormone.

This study reports the effects of the removal of endogenous PTH by thyroparathyroidectomy (TPTX) on the recovery of the reduced renal cAMP response to parathyroid hormone (PTH) in rats with chronically elevated PTH secondary to diets deficient in either vitamin D or calcium. After TPTX and infusion with a calcium-glucose solution of the vitamin D-deficient rat, calcium and PTH fell from 5.8 mg/dl and 2,509 pg/ml, respectively, to 4.8 mg/dl and 160 pg/ml at 48 h. There was a partial restoration of response to PTH, assessed by assay of renal cortical adenylate cyclase activity from 64% of control activity prior to TPTX to 84% of control activity at 48 h. When rats fed the diet deficient in calcium were TPTX, serum PTH fell rapidly from 2,811 to 200 pg/ml at 5 h with no further change at 21 h, whereas calcium did not change (5.3 mg/dl). PTH-dependent adenylate cyclase activity increased from 59% of control activity prior to TPTX to 87% at 5 h and 100% of control activity at 21 h after TPTX. Each diet produced similar increases in the serum level of immunoreactive PTH, and the rate of disappearance of the circulating hormone after TPTX was also similar for both groups of rats. The data indicate a slow, partial recovery of the enzyme response to PTH after TPTX of the vitamin D-deficient rat over the time period studied, whereas the recovery was rapid and complete in rats fed the diet deficient in calcium.

Adenylyl Cyclases↗

PubMed1983

A multiresponse parathyroid hormone assay: an inhibitor has agonist properties in vivo.

Vitamin D-deficient rats subjected to thyroparathyroidectomy (TPTX) were used to evaluate in vivo the biological properties of native bovine parathyroid hormone (bPTH) and chemically synthesized fragments and analogues of the hormone on several parameters of hormone action: calcium and phosphorus fluxes, generation of cyclic adenosine 3',5'-monophosphate (cAMP), and the metabolism of 25-hydroxyvitamin D3 [25(OH)D3]. Vitamin D-deficient rats, after TPTX or sham operation, were intravenously infused with a nutrient containing 7.5 mM CaCl2 for 30 h. During the last 7 h, PTH or one of its analogues was infused intravenously at rates between 0.04 and 20 nmol/h. One hour after the start of the peptide infusion, tritiated 25(OH)D3 was injected. Urine was collected hourly for phosphate and cAMP determinations and, at the end of the experiment, blood was obtained to determine the relative accumulation of tritiated 1,25-dihydroxyvitamin D3 ([3H]1,25(OH)2D3). Infusion of bPTH-(1--84), bPTH-(1--34), human (h)PTH-(1--34), or [Nle8, Nle18, Tyr34]bPTH-(1--34) amide was accompanied by a comparable dose-dependent decrease in plasma phosphate and a dose-dependent increase in plasma calcium and [3H]-1,25(OH)2D3, and urinary excretion of phosphate and cAMP. An evaluation of [Nle8, Nle18, Tyr34]bPTH-(3--34) amide, a potent inhibitor of PTH action in vitro in the renal adenylate cyclase assay, revealed that the analogue possessed weak agonist properties in vivo. The analogue increased excretion of both cAMP and phosphate in the urine, decreased plasma phosphate levels, and increased the accumulation of [3H]-1,25(OH)2D3 in the plasma. This multiparameter model system should aid in the elucidation of the in vivo biological effects of PTH and its analogues.

Animals↗

PubMed1986

Effects of serum calcium and phosphorus on skeletal mineralization in vitamin D-deficient rats.

In the present study, we have evaluated the role of calcium and phosphorus concentrations in serum on the mineralization of bone in the absence of vitamin D. This was accomplished by feeding mother rats and subsequently their pups vitamin D-deficient diets varying in calcium, phosphorus, and lactose content. After 5-7 wk on these diets, serum concentrations of 25-hydroxyvitamin D [25(OH)D] and 1,25-hydroxyvitamin D [1,25(OH)2D] were undetectable. Rats fed a vitamin D-deficient diet containing 0.44% calcium and 0.3% phosphorus showed a serum calcium of 4.9-5.9 mg/dl and a serum phosphorus of 7.3-8.2 mg/dl; rickets (wide epiphysial plates) had developed as well as osteomalacia (wide osteoid seams). Rats maintained on a vitamin D-deficient diet containing 3% calcium and 0.65% phosphorus had normal serum calcium, low serum phosphorus, and severe rickets, but osteomalacia was not seen. Rats fed a diet containing 20% lactose, 4% calcium, and 1% phosphorus showed normal serum calcium, somewhat low serum phosphorus, normal serum PTH, normal width of the epiphysial plate, normal volume density of trabecular bone, and normal volume density of osteoid seams. These data confirm the findings of others, using a different experimental model, that serum calcium and phosphorus concentrations are the determining factors in mineralization defects and not the absence of 25(OH)D or 1,25(OH)2D. In these rats thyroparathyroidectomy is well tolerated, which makes for an ideal model for the study of the effects of calcium-regulating hormones on bone histology, cytology, and biochemistry.

Animals↗

PubMed1991

Homologous amino-terminal radioimmunoassay for rat parathyroid hormone.

Existing radioimmunoassays for parathyroid hormone (PTH) in rat plasma are based on cross-reactivity of rat PTH (rPTH) with heterologous antisera. We used the synthetic NH2-terminal fragment of rPTH [rPTH-(1-34)] to develop a homologous radioimmunoassay for circulating PTH. An antiserum to rPTH-(1-34) was raised in a goat (G-813), and the same peptide was used as radioligand (125I) and standard. Purification of the label by high-performance liquid chromatography (HPLC) increased specific binding greater than twofold and sensitivity by 50-100%. With a final antiserum dilution of 1:70,000, maximum specific binding of 30-33%, nonspecific binding of 1-5%, and 50-microliters sample additions, the assay detection limit was 1.8-2.5 pmol/l. A midregional fragment of human PTH did not displace 125I-labeled rPTH-(1-34). HPLC of extracts of rat parathyroid glands and hyperparathyroid plasma showed only a single peak of immunoreactivity that eluted 2 min after rPTH-(1-34). Dose dilution curves for rat parathyroid gland extracts, rPTH-(1-34) added to rat plasma, and endogenous rat plasma PTH all paralleled the standard curve. Immunoreactive PTH (irPTH) was detectable in greater than 90% of fasting normal rat plasma and changed appropriately in response to hyper- and hypocalcemia induced by low-calcium and vitamin D-deficient diets, injections of calcium and EDTA, and after thyroparathyroidectomy. The normal range for rat plasma irPTH was less than 2.0-12 pmol/l, in general agreement with bioassay results of others. Thus rPTH-(1-34) is an excellent immunogen for raising antisera to rPTH, and assays incorporating it may be of great value in studying rat parathyroid physiology.

Animals↗

PubMed1977

Bone extraction and blood clearance of diphosphonate in the dog.

The transcapillary extraction of diphosphonate, as [99mTc]EHDP, a substance used in bone scanning and for management of certain metabolic bone diseases, has been examined. The maximum instantaneous extraction for [99mTc]EHDP was 0.27 +/- 0.05 (mean +/- SD, N = 10) and the net extraction at 5 min was 0.18 +/- 0.05 (N = 10). The permeability ratio of [99mTc]EHDP to the freely diffusible compound, sucrose, using the formula PS = -Fs loge (1 - Emax), was 0.71. This is similar to the ratio of diffusion coefficients of EHDP to sucrose, which is estimated to be 0.78. These results suggest that the mechanism by which [99mTc]EHDP passes through the capillaries in bone is passive diffusion. Tissue level estimations of EHDP confirm a rapid blood clearance associated with an increase in the rate of urinary excretion; the level of [99mTc]EHDP in bone, however, remains constant. The fractional excretion of [99mTc]EHDP was 27.3 +/- 2.0% in control dogs and was unchanged by thyroparathyroidectomy and subsequent infusion of parathyroid hormone.

Animals↗

PubMed1975

Tetany: quantitative interrelationships between calcium and alkalosis.

Tetany occurs with hypocalcemia and alkalosis or both. The interrelationship of calcium and acid-base balance necessary for inducing tetany, the role of the central nervous system, and the rate of development of hypocalcemia have been investigated. Tetany occurred in less than 50 percent of one group of dogs made alkalotic by hyperventilation or made hypocalcemic by infusion of ethylene glycol-bis(beta-amino ethyl ether) N, N'-tetraacetate. In contrast, hypocalcemia combined with hypocapnic alkalosis always produced tetany. Slowly evolving hypocalcemia was achieved inanother group of dogs by thyroparathyroidectomy, and tetany was induced postoperatively by hypocapnic alkalosis. An identical relationship between serum calcium ion concentration and arterial pH or CO2 tension was found in both groups. Tetany could not be related to the cerebrospinal fluid (CSF) calcium ion content in either group. Hypocalcemia and alkalosis are therefore coparticipants in the development of tetany and are independent of the rate of development of hypocalcemia and of CSF calcium ion concentration. The importance of alkalosis in tetany with hypoparathyroidism is emphasized.

Alkalosis, Respiratory↗

PubMed1976

Relationship between clearances of Ca and Na: effect of distal diuretics and PTH.

One of the objectives of this study was to determine whether or not the absence of parathyroid hormone (PTH) modifies quantitatively the acute action of chlorothiazide (CTZ) to lower the clearance ratio, CCa/CNa. The same group of dogs was studied with standard clearance techniques before and after thyroparathyroidectomy (T-PTX), and after T-PTX during the infusion of PTH. There was no significant difference in the response to CTZ before or after T-PTX, or during the infusion of PTH. The effects of PTH and a maximally effective dose of CTZ were additive. A second objective of this work was to ascertain whether or not two other diuretics which act on the distal tubule, amiloride and triamterene, had actions on CCa/CNa similar to that of CTZ. Amiloride caused a reduction in CCa/CNa which, even at maximally effective doses, was much smaller than the effect of CTZ. Maximally effective doses of amiloride and CTZ had additive actions. Triamterene was evaluated at only one dose; it also lowered the ratio CCa/CNa.

Amiloride↗

PubMed1976

Intrarenal calcium in phosphate handling.

The intrarenal role of plasma ionized calcium (Ca), on fractional phosphate excretion (FE PO4) was investigated in dogs with control of parathyroid hormone (PTH). In series 1, acute thyroparathyroidectomy was immediately followed by a constant infusion of bovine PTH (0.01 U/kg per min). Subsequent calcium chloride infusions increased Cai in plasma phosphate and decreased in the percentage of ultrafiltrable phosphate. A 20% increase in Cai significantly increased FE PO4 by +3.82 +/- 0.97% (P less than 0.01) when infused intravenously and by +2.62 +/- 1.06% (P less than 0.05) when infused in the renal artery. In contrast, a 75% increase in Cai did not significantly change FE PO4. In series 2, dogs were thyroparathyroidectomized 18 h before experiments, and no PTH infusion was initiated. A bolus of bovine PTH (30 U/kg) increased FE PO4 + 8.9 +/- 0.9% (P less than 0.001) in hypocalcemic dogs, +19.1 +/- 4.4% (P less than 0.001) in normolcalcemic dogs, and +15.5 +/- 1.5% (P less than 0.001) in hypercalcemic dogs. We conclude that increases in plasma calcium potentiate the phosphaturic effect of PTH. This potentiating effect is attenuated in marked hypercalcemia by superimposed hemodynamic and/or metabolic changes.

Animals↗

PubMed1976

Regulation of plasma calcium in rats: age-related roles of PTH and calcitonin.

To determine the influence of aging on the relative roles of parathyroid hormone (PTH) and calcitonin in the control of calcium homeostasis during fasting, we assessed changes in plasma calcium in fasted rats following simultaneous removal of the glands that secrete both hormones. Animals ranging in age from 3 to 34.7 wk were thyroparathyroidectomized or sham operated and bled by orbital puncture prior to and 1.5, 3, and 6 h after surgery. After thyroparathyroidectomy (TPTX), plasma calcium fell immediately and progressively in very young rats (3-6 wk old); in young animals (6.5-9.4 wk old), there was a delay of about 1.5 h pceded by a rise, which persisted for at least 3 h. Since the rise and fall in plasma calcium after TPTX are most likely due to calcitonin and PTH deficiencies, respectively, our observations are consistent with the following hypothesis; in the fasting state, the relative importance of calcitonin and PTH in the regulation of plasma calcium varies with age; PTH appears to play the dominant role in young rats; however, during maturation the importance of calcitonin appears to increase progressively.

Age Factors↗

PubMed1979

Endogenous nature of circadian rhythms in calcium metabolism.

Rats studied when the lights are on from 0600 to 1800 daily and fed only in the dark period displayed circadian rhythms in plasma calcium (ionized and total) and 45Ca concentrations, 6 and 8 days after 45Ca administration. In rats fed a calcium-deficient diet, the amplitude of daily variation of plasma ionized and total calcium increased markedly whereas plasma 45Ca daily fluctuation remained essentially unchanged. In the calcium-deficient rats, significant correlations between plasma calcium and 45Ca and between plasma calcium and magnesium were observed throughout the 24 h; circadian periodicity of calcium metabolism persisted in rats fasted overnight, regardless of the illumination schedule. Normal daily fluctuations in plasma 45Ca, lost after thyroparathyroidectomy (TPTX), were restored by feeding the TPTX rats a high-calcium diet. These results demonstrate clearly that circadian rhythms of calcium metabolism occurred irrespective of the light-dark schedule, the calcium supply through intestines and the thyroparathyroid system. An attractive suggestion is that circadian rhythmicity originates as a result of dynamic properties involving nonlinear processes of calcium metabolism.

Animals↗

PubMed1990

A method for continual monitoring of bone resorption in rats: evidence for a diurnal rhythm.

A method has been developed to monitor bone resorption (BR) based on the urinary excretion of [3H]tetracycline ([3H]TC) from chronically prelabeled rats. This is possible because the [3H]TC released from bone has been found to be in a form that is not or only poorly bound to apatite and thus not reincorporated into newly formed bone. When BR was increased by means of dietary calcium restriction, parathyroid hormone (PTH) infusion, or retinoid injections, urinary [3H]TC doubled. When BR was inhibited by feeding calcium supplements or administration of dichloromethylenebisphosphonate, [3H]TC excretion dropped by two-thirds. Thyroparathyroidectomy inhibited [3H]TC excretion by one-third. The results obtained with this technique are therefore similar to those obtained with other methods such as 45Ca kinetics. The effect of dietary manipulations on BR was detected within 6 h of changing diet. Furthermore, a strong diet-dependent but PTH- and calcitonin-independent diurnal rhythm in BR was found. By use of this technique, bone resorption can be assessed continuously over long periods, and the acute regulation of bone resorption can be studied for the first time.

Animals↗

PubMed1993

Independence of salt intake from the hormones regulating calcium homeostasis.

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.

Animals↗

PubMed2004

Regulation of renal NaPi-2 expression and tubular phosphate reabsorption by growth hormone in the juvenile rat.

Growth hormone (GH) is an important factor in the developmental adaptation to enhance P(i) reabsorption; however, the nephron sites and mechanisms by which GH regulates renal P(i) uptake remain unclear and are the focus of the present study. Micropuncture experiments were performed after acute thyroparathyroidectomy in the presence and absence of parathyroid hormone (PTH) in adult (14- to 17-wk old), juvenile (4-wk old), and GH-suppressed juvenile male rats. While the phosphaturic effect of PTH was blunted in the juvenile rat compared with the adult, suppression of GH in the juvenile restored fractional P(i) excretion to adult levels. In the presence or absence of PTH, GH suppression in the juvenile rat caused a significant increase in the fractional P(i) delivery to the late proximal convoluted (PCT) and early distal tubule, so that delivery was not different from that in adults. These data were confirmed by P(i) uptake studies into brush-border membrane (BBM) vesicles. Immunofluorescence studies indicate increased BBM type IIa NaP(i) cotransporter (NaPi-2) expression in the juvenile compared with adult rat, and GH suppression reduced NaPi-2 expression to levels observed in the adult. GH replacement in the [N-acetyl-Tyr(1)-d-Arg(2)]-GRF-(1-29)-NH(2)-treated juveniles restored high NaPi-2 expression and P(i) uptake. Together, these novel results demonstrate that the presence of GH in the juvenile animal is crucial for the early developmental upregulation of BBM NaPi-2 and, most importantly, describe the enhanced P(i) reabsorption along the PCT and proximal straight nephron segments in the juvenile rat.

Animals↗

PubMed1978

Glucose-mediated inhibition of phosphate reabsorption in rat kidney.

Clearance, tracer intra-arterial injection, and tracer intratubular microinjection techniques were used on two strains of Wistar rats. In Saclay rats, clearance studies during hyperphosphatemia showed that glucose significantly decreased reabsorption of phosphate; during normal phosphatemia, glucose induced a 25% inhibition both in nondiuretic and in volume-expanded animals; thyroparathyroidectomy did not modify this inhibition. When mannitol was substituted for glucose, no change in phosphate reabsorption was noted. Tracer injection into the renal arteries of [3H]inulin, [14C]glucose, and [32P]-phosphate with or without additional unlabeled glucose or mannitol showed that the presence of glucose significantly increased 14C and 32P urinary recoveries but not mannitol. Intratubular paired microinjections into early proximal tubules of the same tracers with and without glucose showed that addition of sugar also increased the 14C and 32P urinary recoveries. In Munich rats, the effects were much less marked than in Saclay rats. It is concluded that the inhibitory effect of glucose 1) partly results from intrarenal factors, 2) is linked to glucose reabsorption per se but not to a nonspecific osmotic intraluminal effect, 3) is localized on the tubular luminal side, and 4) is subject to strain differences.

Animals↗

PubMed1979

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

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.

Animals↗

PubMed1979

Phosphate transport along the inner medullary collecting duct of the rat.

The question of phosphate transport along the collecting duct remains controversial inasmuch as no data from direct in vivo evaluation of this nephron segment have been reported. We measured net phosphate transport along the inner medullary collecting duct (IMCD) using the collecting duct microcatheterization technique in five groups of rats. In control rats no net phosphate transport was found and 9.4% of the fraction of filtered phosphate (FFP) entered the IMCD and was excreted. After acute thyroparathyroidectomy (TPTX) there was a striking reduction in the FFP entering the IMCD, 1.8%, and significant reabsorption occurred, 0.5% being excreted. With acute TPTX and parathormone infusion, delivery increased to 33% without significant change along the IMCD. With acute TPTX and phosphate infusion, delivery was increased to control levels but no change was found in net phosphate transport. In rats studied 5-7 days after uninephrectomy alone, phosphate delivery was greater than in control, 25%, and no net phosphate transport was found. These studies demonstrate that phosphate absorption occurs along the IMCD in acutely TPTX rats when the delivery of phosphate to the IMCD is markedly reduced. The increase in phosphaturia which occurs after a reduction in renal mass cannot be accounted for by changes in net phosphate transport along the IMCD.

Animals↗

PubMed1980

Calcium and magnesium transport along the inner medullary collecting duct of the rat.

We have measured calcium and magnesium transport along the inner medullary collecting duct (IMCD) in rats by the microcatheterization technique. The fraction of filtered divalent cation ((F/P)Ca,Mg/In) as a function of IMCD length was analyzed by linear regression. In eight control rats calcium reabsorption was demonstrated, inasmuch as there was a significant correlation and slope, P less than 0.001. (F/P)Ca/In decreased from 2.2 +/- 0.3% at the beginning of the IMCD to 0,84 +/- 0.1% in the urine. (F/P)Mg/In was not changed along the IMCD, After acute thyroparathyroidectomy (TPTX) (F/P)Ca/In increased to 4.6 +/- 0.4% at the beginning of the IMCD and 1.55 +/- 0.1% in the urine. The slope was not significantly different from the control group. (F/P)Mg/In was unchanged and was not different from the control group. Accordingly, net Ca reabsorption occurs along the IMCD and the fractional Ca reabsorption is not altered by TPTX. Net Mg transport along the IMCD was absent in both control and TPTX rats; The increased calciuresis after TPTX is not dependent on IMCD function nor is Mg excretion under the conditions studied.

Animals↗