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PubMed1980

Effects of PTH, ADH, and cyclic AMP on distal tubular Ca and Na reabsorption.

Tubular microperfusion experiments were performed in rats to examine the effects of thyroparathyroidectomy (TPTX), parathyroid hormone (PTH), antidiuretic hormone (ADH), and cyclic AMP (cAMP) on distal tubular Ca, Na, and water reabsorption. TPTX caused a significant decrease in the Ca reabsorptive rate as compared to intact animals. PTH (5 U/kg; 2 U x kg-1 x h-1) replacement in TPTX animals restored Ca transport to control levels. Application of either cAMP (10(-3) M) or 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (10(-5) M) to the surface of the kidney caused a stimulation of Ca reabsorption similar to that produced by PTH. Neither TPTX nor PTH changed Na or water reabsorption significantly, whereas the cyclic nucleotides increased both of these parameters. These later actions of cAMP duplicated effects of ADH observed in these distal tubules.

Animals↗

PubMed1981

Tubular transport and urinary excretion of phosphate after renal denervation in the anesthetized rat.

Tubular transport of phosphate (Pi) was studied using clearance and tracer microinjection techniques in Inactin-anesthetized male rats subjected to left kidney denervation. Experiments were conducted in the following groups: i) acute denervation (AD); ii) chronic denervation (CD); iii) acute denervation plus thyroparathyroidectomy (AD + TPTX); iv) microinjection with AD. Besides a marked diuresis and natriuresis with no difference in GFR between innervated (inn) and denervated (den) kidneys, unilateral renal denervation resulted in an increased urinary excretion and decreased tubular reabsorption of inorganic phosphate. Maximum tubular reabsorption of Pi (TmPi) calculated per unit GFR was (means +/- SE): AD, inn: 2.38 +/- 0.04, den: 1.98 +/- 0.06 mumol/ml; CD, inn: 2.66 +/- 0.10, den: 2.19 +/- 0.11 mumol/ml; AD + TPTX, inn: 4.78 +/- 0.06, den: 4.26 +/- 0.08 mumol/ml. Thus, differences in TmPi between the two sides were of the same magnitude in the three groups. Fractional recovery of 32Pi from microinjections in control (C) and postdenervation (D) periods was: early proximal, C: 53.0 +/- 0.81, D: 61.3 +/- 1.07%; late proximal, C: 77.0 +/- 0.81, D: 70.6 +/- 0.60%; early distal, C: 93.7 +/- 0.75, D: 03.5 +/- 0.72%. It is concluded that renal sympathectomy depresses tubular transport of inorganic phosphate in anesthetized rats by a primary action on the proximal convoluted tubule and with a partial compensation in the loop of Henle.

Animals↗

PubMed1981

Renal and systemic acid-base effects of chronic hypoparathyroidism in dogs.

MEtabolic alkalosis has been reported in patients with chronic hypoparathyroidism under conditions of uncontrolled diet and medication intake. Hypoparathyroidism has also been reported to result in increased renal bicarbonate reabsorptive capacity in acutely bicarbonate-loaded dogs. However, the acid-base effects of experimentally induced chronic hypoparathyroidism have not been investigated in any species. Accordingly, we investigated the chronic effects of hypoparathyroidism by thyroparathyroidectomy (TPTX) plus thyroxine replacement on renal regulation of plasma acid-base composition under metabolic balance conditions of normal dietary acid load (group I) and alkali load (group II, 9.0 meq/kg HCO3(-) daily) in dogs ingesting a normal Cl-, high Ca2+ diet throughout study. For groups I and II pre-TPTX: [HCO3(-)]p, 19.7 +/- 1.0, 20.1 +/- 0.9 meq/liter. Plasma acid-base composition (days 5-10) was unchanged by TPTX: delta [HCO3(-)]p, -0.7 +/- 0.4, 0.0 +/- 0.2 meq/liter; delta [H+]p, 0 +/- 1, -1 +/- 0 neq/liter, NS from control. A reduction in plasma total calcium concentration ([CaT]p) occurred and persisted (group I: [CaT]p, -1.6 +/- 0.2 mg/100 ml, P less than 0.01, day 1 and -1.2 +/- 0.9, days 5-10; group II: -1.4 +/- 0.3 mg/100 ml, P less than 0.01, day 1 and -2.3 +/- 0.4, days 5-10). No significant change in net acid or Cl- excretion occurred following TPTX. Thus, chronic hypoparathyroidism characterized by a chronic reduction in [CaT]p does not result in significant alterations in renal regulation of plasma acid-base composition in the dog.

Acid-Base Imbalance↗

PubMed1982

Independence of the acute acid-buffering response from endogenous parathyroid hormone.

Two recent reports have made the provocative suggestion that parathyroid hormone (PTH) and, by implication, bone play a critical role in the early phase of acid buffering. The purpose of the present study was to investigate the effect of PTH on the acute buffering process by examining the influence of thyroparathyroidectomy (TPTX) on acid-base parameters in nephrectomized rats following infusion of hydrochloric acid at two differing doses. To ensure hemodynamic and physiologic stability of the animals, the required surgical procedures were staged over several days. Additionally, the experimental protocol was carried out in awake and unrestrained animals. Non-TPTX (sham) animals underwent a sham operation to equalize the surgical stresses between the two groups. The decrements in plasma [HCO-3] observed following infusion of 3.5 mmol/kg HCl over 1 h did not differ between TPTX vs. sham animals at 1 h (-9.4 vs. -9.9 meq/liter), 3 h (-8.6 vs. 8.6 meq/liter), or 6 h (-8.6 vs. -8.5 meq/liter) from the start of the infusion. Similarly, virtually identical falls in plasma [HCO-3] were observed between TPTX vs. sham rats after infusion of 5 mmol/kg HCl over 30 min at 30 min (-13.6 vs. -14.2 meq/liter) and 3 h (-10.9 vs. -11.4 meq/liter) after the start of the infusion. At both doses, the resultant changes in plasma [H+] and PaCO2 were not different in the two groups. The observed mortality was comparable in both TPTX and sham groups. The data demonstrate that endogenous PTH is not necessary in the early phase of buffering of a mineral acid load.

Acid-Base Equilibrium↗

PubMed1983

Effects of calcitonin on the renal concentrating mechanism.

The effects of salmon calcitonin on the renal concentrating mechanism were investigated in homozygous DI Brattleboro rats. The levels of peptide hormones believed to produce the same physiological responses as antidiuretic hormone on the thick ascending limb (glucagon, parathyroid hormone, and calcitonin) and the cortical collecting ducts (calcitonin) were reduced by acute thyroparathyroidectomy and somatostatin administration. In these hormone-deprived animals, the corticomedullary concentration gradient was almost abolished; the (F/P)osmol at the tip of the juxtamedullary nephrons was 1.19 +/- 0.05. Calcitonin administration restored the gradient [(F/P)osmol = 1.85 +/- 0.14] and simultaneously absolute and fractional water excretion fell significantly despite the concomitant rise in the glomerular filtration rate. It is concluded that 1) in the hormone-deprived animal, calcitonin administration consistently enhances the corticomedullary concentration gradient, and 2) the effects of hormone deprivation and calcitonin administration on the urinary concentrating mechanism are compatible with direct stimulation by calcitonin of electrolyte reabsorption along the thick ascending limb and/or of the water permeability of the cortical collecting ducts.

Animals↗

PubMed1984

Critical role of extracellular calcium in vanadate-induced renal vasoconstriction.

Intra-arterial infusion of vanadate (VO4) in dogs produces a reduction in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow (V), and the fractional excretion of sodium (FENa+). To evaluate the role of Ca2+ in these changes VO4 was infused into the renal artery in the presence of the calcium antagonists trifluoperazine (TFP), verapamil, or EGTA. TFP inhibited the effect of VO4 on RBF (TFP + VO4:64.1, VO4:38.5 ml/min; P less than 0.05), GFR (TFP + VO4:22.9, VO4:9.3, ml/min; P less than 0.05) and V (TFP + VO4: 0.80, VO4: 0.38 ml/min; P less than 0.05) without changing FENa+ (TFP + VO4: 3.8, VO4: 3.2%). Similar changes were obtained with verapamil as well as with EGTA. Furthermore thyroparathyroidectomy (TPTX) decreased serum calcium (control: 8.78, TPTX: 4.98 mg/100 ml; P less than 0.05) and blunted the effects of VO4 on renal hemodynamics. Reestablishing normal serum Ca2+ by an intra-arterial infusion of CaCl2 elicited the VO4 effects of vasoconstriction and decreased GFR; V was not affected and FENa+ rose. The data support the idea that influx of extracellular calcium into smooth muscle cells mediates the hemodynamic effects of VO4 in the dog.

Animals↗

PubMed2000

PTH regulates expression of ClC-5 chloride channel in the kidney.

Mutations in the chloride channel, ClC-5, have been described in several inherited diseases that result in the formation of kidney stones. To determine whether ClC-5 is also involved in calcium homeostasis, we investigated whether ClC-5 mRNA and protein expression are modulated in rats deficient in 1alpha,25(OH)(2) vitamin D(3) with and without thyroparathyroidectomy. Parathyroid hormone (PTH) was replaced in some animals. Vitamin D-deficient, thyroparathyrodectomized rats had lower serum and higher urinary calcium concentrations compared with control animals as well as lower serum PTH and calcitonin concentrations. ClC-5 mRNA and protein levels in the cortex decrease in vitamin D-deficient, thyroparathyroidectomized rats compared with both control and vitamin D-deficient animals. ClC-5 mRNA and protein expression increase near to control levels in vitamin D-deficient, thyroparathyroidectomized rats injected with PTH. No significant changes in ClC-5 mRNA and protein expression in the medulla were detected in any experimental group. Our results suggest that PTH modulates the expression of ClC-5 in the kidney cortex and that neither 1alpha,25(OH)(2) vitamin D(3) nor PTH regulates ClC-5 expression in the medulla. The pattern of expression of ClC-5 varies with urinary calcium. Animals with higher urinary calcium concentrations have lower levels of ClC-5 mRNA and protein expression, suggesting that the ClC-5 chloride channel plays a role in calcium reabsorption.

Animals↗

PubMed2001

Parathyroid hormone-1 receptor down-regulation in kidneys from rats with chronic renal failure.

Although secondary hyperparathyroidism is a common complication of chronic renal failure, few studies have examined the characteristics of parathyroid hormone (PTH) binding to the kidney or the regulation of the PTH receptor in chronic renal disease. In this study we measured PTH binding to the PTH-1 receptor in renal cortical membranes from normal rats and from rats with experimentally induced chronic renal failure. In normal rats, analysis of saturation binding experiments using 125I PTH-related peptide (chicken, cPTHrP) revealed apparent Kd and Bmax values of 1.16 +/- 0.14 nmol/l and 338 +/- 22.7 fmol/mg, respectively. Three weeks following induction of renal failure there was no change in the affinity of the PTH-1 receptor (Kd = 1.51 +/- 0.24 nmol/l) but the Bmax was reduced by 45% (183 +/- 32.5). In normal rats which had undergone thyroparathyroidectomy, the Kd was unchanged (1.17 +/- 0.09) while the Bmax increased to 459 +/- 31 fmol/mg. We conclude that chronic renal failure is accompanied by a downregulation of renal PTH-1 receptors.

Animals↗

PubMed1982

Interactions of starvation and selective phosphorus depletion on renal phosphate reabsorption.

Renal phosphate (Pi) wastage following 7 days of starvation was investigated in normal rats (HI-P) and others previously stabilized on a low phosphorus (LO-P)diet. In LO-P animals, Pi excretion increased after starvation, but was significantly less than in starved HI-P rats. After thyroparathyroidectomy, the increase in Pi excretion after parathyroid hormone (PTH) was significantly greater in nonacidotic starved HI-P rats than in LO-P animals. However, PTH elicited a 31-fold increase in Pi excretion in both of these groups. Starved LO-P and HI-P rats responded equivalently to dibutyryl cyclic AMP. The renal response to phosphate depletion normally promotes Pi conservation, but is attenuated markedly by 7 days of subsequent starvation. This results from at least partial restoration of phosphaturic responsiveness to PTH during starvation.

Animals↗

PubMed1985

Effects of changes in serum calcium and parathyroid hormone on plasma renin in intact mongrel dogs.

Studies were undertaken to extend previous experiments of the interaction between calcium and parathyroid hormone on renin synthesis by the kidney. Intact normovolemic mongrel dogs between 15 and 25 kg were used for all studies. Plasma renin activity (PRA) was measured by radioimmunoassay. Hypocalcemia produced by thyroparathyroidectomy or chelation with EDTA resulted in an elevated PRA of 3.76 +/- 0.85 ng/ml/h in 17 normotensive dogs compared to 1.52 +/- 0.29 ng/ml/h in 14 normocalcemic normotensive dogs (p less than 0.05). In 5 renovascular dogs, calcium-channel antagonism with nifedipine resulted in a higher PRA of 31.8 +/- 0.5 compared to 11.9 +/- 1.1 ng/ml/h in 23 control renovascular dogs not receiving nifedipine (p less than 0.001). The reactive hyperreninemia following angiotensin blockade was greater in 22 hypocalcemic (10.94 +/- 2.03 ng/ml/h) normotensive dogs compared to 14 normocalcemic normotensive dogs (1.32 +/- 0.34 ng/ml/h, p less than 0.001). Similar results were obtained with angiotensin blockade in nifedipine-treated animals compared to angiotensin blockade in nonnifedipine-treated normotensive dogs. Results with angiotensin blockade on PRA levels in renovascular dogs were found similar to those described with angiotensin blockade in normotensive dogs. We conclude from these studies that calcium reduction, independent of a rise in parathyroid hormone, or calcium-channel blockade was associated with an elevation of PRA in normotensive and renovascular hypertensive dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Effect of parathyroid hormone on antioxidant enzyme activity and lipid peroxidation of erythrocytes in five-sixths nephrectomized rats.

The purpose of the study was to investigate the effects of parathyroid hormone (PTH) infusion on antioxidant enzyme activity and lipid peroxidation of erythrocytes in five-sixths nephrectomized (Nx) rats. Five-sixths Nx rats had a higher osmotic fragility in red blood cells (RBC). Thyroparathyroidectomy (TPTX) effectively decreased the abnormality of osmotic fragility in RBC in Nx rats. PTH infusion in Nx-TPTX rats markedly increased the osmotic fragility in RBC. Total glutathione was measured by using the enzyme-recycling method. We found elevated glutathione levels in RBC of five-sixths Nx rats, but this elevation could be inhibited by TPTX and recovered by PTH infusion in Nx-TPTX rats. Five-sixths Nx rats had a lower glutathione peroxidase activity in RBC, but TPTX or PTH infusion was not found to alter the decrease of the glutathione peroxidase activity in RBC of five-sixths Nx rats. These rats had a higher activity in RBC superoxide dismutase as compared with sham-operated controls (p < 0.05), but the higher activity in RBC superoxide dismutase in Nx rats had been inhibited by TPTX. PTH infusion recovered the higher activity in RBC superoxide dismutase in five-sixths Nx-TPTX rats. Nx rats were not found to alter the activity of catalase in RBC. Neither could TPTX or PTH infusion in Nx rats influence the activity of catalase in RBC. A high lipid peroxidation in RBC was found in five-sixths Nx rats, namely, increased formation of malondialdehyde (MDA) in RBC had been induced to produce lipid peroxidation by H2O2, but neither TPTX nor PTH infusion could inhibit or enhance the increase of lipid peroxidation in RBC of Nx rats. These results indicate that PTH infusion did not increase the susceptibility to lipid peroxidation in RBC of five-sixths Nx rats. Thus, the increased osmotic fragility in RBC induced by PTH infusion may not result from the reduction in the RBC defense mechanism against free radical toxicity.

Animals↗

PubMed1980

Effects of parathyroid hormone on glomerular function.

Acute thyroparathyroidectomy (TPTX) in rats results in a marked increase in the glomerular capillary ultrafiltration coefficient, Kf. Infusion of a submaximal dose of bovine PTH (1 U/kg/min) returns Kf to non-TPTX levels. Infusion of 10 U/kg/min of bovine PTH further reduces Kf and leads to a net reduction in single nephron GFR. These findings suggest that PTH may play an important role in modulating Kf and, consequently, GFR.

Animals↗

PubMed1970

Evidence for suppression of parathyroid gland activity by hypermagnesemia.

The effect of hypermagnesemia, produced by MgCl(2) infusion, on the activity of parathyroid glands, as assessed by changes in levels of serum calcium (S(Ca)) and in the fraction of filtered phosphate excreted (C(P)/C(Cr)), was studied in 11 intact and 4 thyroparathyroidectomized (T-PTX) dogs. To exclude the effect of diurnal variation in C(P)/C(Cr) on the results, studies were initiated in both morning and afternoon hours and each study with MgCl(2) infusion was paired with a control experiment in the same dog not receiving MgCl(2). During MgCl(2) infusion, serum phosphorus rose progressively. Despite this rise, the levels of C(P)/C(Cr) fell in all experiments and were significantly different from values observed at the same time of the day in the paired control experiments. The concentrations of total S(Ca) fell by 1.0-2.4 mg/100 ml with a proportional decrease in the levels of the diffusible and ionized fractions. The pattern of the fall in C(P)/C(Cr) during MgCl(2) resembled that observed after CaCl(2) infusion (seven dogs) and that which acutely followed thyroparathyroidectomy (seven dogs). When parathyroid extract was given to dogs receiving MgCl(2) infusion both C(P)/C(Cr) and S(Ca) rose, and MgCl(2) infusion did not affect C(P)/C(Cr) and S(Ca) in T-PTX dogs. These results indicate that hypermagnesemia suppresses the activity of the parathyroid glands, probably, by inhibiting production and (or) release of the hormone, without interfering with end-organ response. An increase in serum magnesium of 1.7-2.0 mg/100 ml was capable of producing the suppressive effect. Evaluation of the effect of simultaneous modest hypocalcemia and hypermagnesemia suggests that a decrease in the level of serum calcium is more potent than an increase in the concentration of serum magnesium in the regulation of parathyroid activity.

Animals↗

PubMed1971

Pathogenesis of hypocalcemia in magnesium depletion. Normal end-organ responsiveness to parathyroid hormone.

Hypocalcemia in the hypomagnesemic state in man is usually attributed to refractoriness of end-organs to the calcemic action of parathyroid hormone. We studied the responsiveness of end-organs to bovine parathyroid extract (PTE) in magnesium-depleted and control dogs by the following three methods after thyroparathyroidectomy: (a) assessment of the calcemic response to a set dose of PTE (0.3 U/kg per hr); (b) assessment of PTE dose required to attain normocalcemia; (c) evaluation of regression lines of plasma calcium concentration on PTE dose. The calcemic response of magnesium-depleted thyroparathyroidectomized puppies to a set dose of PTE was similar to that of control puppies. There was no significant difference in the dose of PTE required to attain normocalcemia nor in the dose-response relations between the plasma calcium concentration and the PTE dose. In a group of magnesium-depleted puppies with intact thyroid and parathyroid glands, the dose of PTE required to attain normocalcemia was similar to that required in thyroparathyroidectomized animals, indicating calcitonin was not a factor contributing to hypocalcemia. We conclude that hypocalcemia in magnesium-depleted puppies is not due to refractoriness of end-organs to the calcium-mobilizing action of parathyroid hormone. Defective synthesis or diminished secretion of parathyroid hormone is suggested as an explanation.

Alkaline Phosphatase↗

PubMed1974

Calcium metabolism of brain in acute renal failure. Effects of uremia, hemodialysis, and parathyroid hormone.

Studies were carried out to evaluate the changes in content of calcium and magnesium in brain during acute uremia in dogs. Ca content in gray and white matter of brain increased significantly after 3 days of acute uremia and this increment was prevented by thyroparathyroidectomy (TPTX). The administration of parathyroid extract (PTE) to normal dogs and TPTX uremic animals produced a significant rise in brain Ca. These changes were not related to alteration in the concentration of Ca in plasma or cerebrospinal fluid, to changes in calcium-phosphorus product, or to changes in blood pH. Furthermore, the infusion of large amounts of phosphate to vitamin D2-treated animals with suppressed parathyroid gland activity produced marked elevation in calcium-phosphorus product but no significant change in brain Ca. Also, uremia in vitamin D2-treated TPTX dogs failed to increase calcium content in brain despite marked elevation in calcium-phosphorus product. Hemodialysis significantly reduced Ca content of brain but the values were still significantly higher than normal. Mg content increased modestly only in the white matter of uremic dogs with intact parathyroid glands and in normal dogs and TPTX uremic dogs receiving PTE. The results indicate that (a) acute uremia of 3 days is associated with a marked rise of Ca content of brain and modest increment of Mg in certain parts of the brain, and (b) these alterations are not related to uremia, per se, but are dependent on the presence of excess parathyroid hormone. It is suggested that the neurological abnormalities noted in acute uremia may be related in part to the rise in the Ca content of brain.

Acute Disease↗

PubMed1975

Evidence for physiological importance of calcitonin in the regulation of plasma calcium in rats.

To determine the physiological importance of calcitonin in the regulation of plasma calcium, studies were carried out in fasting animals to (a) assess the acute effects of thyroparathyroidectomy (TPTX) and thyroidectomy (TX) on plasma and urinary calcium; (b) investigate whether the changes in plasma calcium produced by removal of the glands were dependent on the presence of the kidney; and (c) determine if the effect of TPTX on plasma calcium is affected by age. Except where otherwise indicated, all studies were carried out on fasting male Wistar rats weighing over 300 g. The following observations were made. (a) TPTX and TX caused an increase in plasma calcium in nephrectomized animals. (b) This increase was not dependent on nephrectomy since in intact animals bearing autoparathyroid transplants TX also caused a significant rise in the mean plasma calcium level (0.37 mg/100 ml at 1 1/2 h). (c) Urinary calcium increased twofold in the 3-h period immediately after TX. (d) In unnephrectomized immature (50-g) rats, TPTX caused a progressive decrease in plasma calcium in contrast to old (360-g) rats, where a significant fall observed at 6 h was preceded by an increase in plasma calcium (0.5 mg/100 ml at 1 1/2 h). From these observations we conclude that: (a) calcitonin must play an important physiological role in the regulation of plasma calcium since the termination of its basal secretion caused an immediate but transient increase in plasma calcium in old unfed rats; (b) the relative importance of calcitonin and parathyroid hormone in the acute regulation of plasma calcium is age-related; and (c) the action of parathyroid hormone on bone may be modified by changes in ambient calcitonin concentration.

Aging↗

PubMed1976

Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat.

Inorganic phosphate (Pi) reabsorption was studied during Pi infusion, after acute or chronic thyroparathyroidectomy (TPTX), in rats stabilized on a high-phosphorus (1% P) or a low-phosphorus (0.02% P) diet. After acute TPTX, there were no consistent differences in Pi reabsorption between the high- and low-phosphorus dietary groups. After chronic TPTX, the rats stabilized on the low-phosphorus diet exhibited nearly complete Pi reabsorption at every plasma Pi level, while the animals receiving the high-phosphorus diet manifested a marked phosphaturic response to Pi infusion. In addition, Pi reabsorption was significantly increased in the chronic TPTX low-phosphorus rats which achieved the highest filtered Pi loads, while their urine remained essentially phosphate-free. Dietary phosphorus-dependent alterations in Pi reabsorption may play a significant role in establishing the rate of Pi excretion per nephron under certain circumstances and should be considered in the interpretation of studies investigating renal Pi handling. The ability of phosphorus-depleted animals to maintain a phosphate-free urine during Pi loading would favor the rapid repletion of body phosphorus stores.

Absorption↗

PubMed1977

Role of 1,25-dihydroxyvitamin D3 on intestinal phosphate absorption in rats with a normal vitamin D supply.

In vitamin D-deficient rats, impaired intestinal phosphorus (P) absorption can be corrected by 1,25-dihydroxyvitamin D(3)[1,25-(OH)(2)D(3)]. In the present study, it was investigated whether changes in 1,25-(OH)(2)D(3) production can influence intestinal P transport also in animals with a normal supply of vitamin D. The intestinal P absorption was evaluated in rats using both the in situ duodenal loop technique and the determination of the overall gastrointestinal absorption under three conditions known to influence the production of 1,25-(OH)(2)D(3): (a) variation in dietary P, (b) thyroparathyroidectomy (TPTX) with or without administration of parathyroid hormone (PTH), and (c) treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). In all circumstances changes in duodenal absorption paralleled the changes in the overall fractional absorption. (a) Lowering dietary P stimulated P absorption. (b) TPTX decreased P absorption. This effect was corrected either by the administration of PTH or by the administration of 1,25-(OH)(2)D(3). (c) EHDP, when given at a dose known to inhibit 1,25-(OH)(2)D(3) formation, decreased the duodenal P absorption in both intact and TPTX animals. This effect was corrected by 1,25-(OH)(2)D(3). In the TPTX-EHDP-treated animals, the administration of PTH did not rectify the low duodenal P absorption. These results support the thesis that, in rats with normal vitamin D supply, variations in the endogenous production of 1,25-(OH)(2)D(3) change the rate of P absorption. However, these changes are in such magnitude that they are of relatively small importance when compared to the effect of variation in the dietary intake of P. These results also strongly suggest that the action of PTH on duodenal P transport is mediated by its effect on 1,25-(OH)(2)D(3) production, inasmuch as the effect of the hormone is abolished after blocking the renal 1-hydroxylation with EHDP.

Animals↗