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PubMed1993

Thyroid and thyroxine effects on adrenoreceptors in relation to circadian activity.

Experiments were conducted to ascertain if changes in central adrenergic receptors could be associated with altered circadian activity patterns induced by thyroparathyroidectomy (TPX) and thyroxine. An initial experiment used TPX and sham-operated rats that had been exposed to dim red light for 7 months. The alpha and beta receptor densities were compared in the suprachiasmatic nuclei (SCN), preoptic (PO), septum, and caudate-putamen. TPX animals showed significant reductions in beta 1 and beta 2 receptor densities in SCN and PO, and alpha 1 densities in SCN, but no other changes. A second experiment, lasting 4 months, examined the effects of thyroxine, which has been shown to reverse the period-shortening effects of TPX surgery. Thyroxine significantly increased beta 1 receptors in both the SCN and ventromedial hypothalamus (VMH), the only regions that displayed significant reductions in TPXs during the second experiment. Increases of sevenfold and threefold were observed in the SCNs of TPXs and shams, respectively, but thyroxine's action in the VMH was limited to TPX animals, an effect that mimics thyroxine's action on circadian activity rhythms.

Animals↗

PubMed1992

Parathyroid gland hormones in the skeletal development of the ovine foetus: the effect of parathyroidectomy with calcium and phosphate infusion.

It has been confirmed that the foetal parathyroid glands are important in development and that thyroparathyroidectomy (TXPTX) of the ovine foetus with thyroxine (T4) replacement leads to hypocalcaemia, retarded skeletal development, depressed calcification and rickets, relative to thyroidectomy plus T4 replacement. Histomorphometric and biochemical (urinary excretion of deoxypyridinoline) indices of bone resorption are also reduced. However, skeletal calcification can be restored to normal by long-term infusion of the TXPTX foetuses with phosphate and calcium sufficient to normalise the plasma Ca2+ x Pi ion product. Nevertheless, depressed resorption, reduced osteoblast numbers and delayed development persisted. The evidence suggests that the abnormally low number of resorption cavities and osteoclasts may result from the reduction in circulatory parathyroid-hormone-related protein consequent upon the removal of the foetal parathyroid glands and that this hypercalcaemic factor has a direct effect upon the process of resorption and primary trabecular remodelling of the foetal skeleton.

Amino Acids↗

PubMed1984

Tissue producing the serum factor stimulating the release of cathepsin D from lysosomes in vitro.

Pancreatectomy as well as thyroparathyroidectomy resulted in the quick disappearance of a serum factor (stimulating cathepsin D release from lysosomes in vitro) from the rat or mouse blood. Extirpation of other organs such as duodenum, stomach, spleen, kidney, submaxillary gland, testis, adrenal gland or hypophysis, showed no effect on the serum factor level. Glucagon (but not insulin or thyroxine) given to the pancreatectomized animals restored the serum factor level in a dose-dependent manner. The serum factor-like activity was detected only in the parathyroids (but not thyroid), and the release of activity from parathyroid-slices was stimulated by glucagon, suggesting that the parathyroid may produce and/or secrete the serum factor under the influence of glucagon.

Animals↗

PubMed1988

A new immunoblotting assay for thymidylate synthetase and its application to the regulation of enzyme activity in regenerating rat liver.

A highly sensitive and specific immunoblot assay has been developed to quantitate the content of rat liver thymidylate synthetase (EC 2.1.1.45). Applying the method, it is demonstrated that the increase of the activity of thymidylate synthetase in liver regeneration after partial hepatectomy is due to the de novo synthesis of the enzyme protein. Administration of cycloheximide, phenoxybenzamine, phorbol 12-myristate 13-acetate, nifedipine, dexamethasone or indomethacin to partially hepatectomized rats prevented the synthesis of thymidylate synthetase in regenerating liver. Thyroparathyroidectomy also inhibited the increase of the enzyme in liver regeneration. These observations are discussed in relation to the signal transduction concerning the alpha 1-receptor, which was shown to regulate liver regeneration in our previous papers.

Animals↗

PubMed1986

Effect of age on parathyroid hormone and forskolin stimulated adenylate cyclase and protein kinase activity in the renal cortex.

The capacity of parathyroid hormone (PTH) to stimulate the renal production of 1,25-dihydroxyvitamin D declines with age. Since the action of PTH in the kidney is mediated by cAMP, we have examined the effect of PTH and forskolin on renal cortical adenylate cyclase in young (3 months), adult (13-15 months), and old (25-27 months) F344 rats. PTH-dependent adenylate cyclase, measured as cAMP accumulation in cortical slices, was reduced in adult and old rats compared to young rats over a PTH concentration range of 0.015-15 units/ml. There was no difference in PTH-dependent adenylate cyclase activity between adult and old rats. Renal plasma membrane preparations demonstrated similar changes in PTH-stimulated adenylate cyclase activity. There was no difference in calcitonin, forskolin, or guanyl-5-ylimidodiphosphate (Gpp(NH)p) stimulation of adenylate cyclase in plasma membranes from each age group, suggesting that the defect lies in the membrane receptor for PTH. The decreased adult sensitivity to PTH could be reversed by thyroparathyroidectomy. PTH stimulation of cytosolic protein kinase activity did not change with age. These results suggest that the decrease in PTH-dependent adenylate cyclase is due to the alterations at the level of PTH receptor. These alterations may be in response to the increase in serum PTH seen in these animals with increasing age.

Adenylyl Cyclases↗

PubMed2005

Calcimimetic NPS R-568 induces hypotensive effect in spontaneously hypertensive rats.

BACKGROUND: The discovery of calcium receptors and calcimimetics created the possibility of "pharmacologic parathyroidectomy" (phPTX), which decreased secretion of parathormone (PTH). Parathyroid glands of spontaneously hypertensive rats (SHR) and of patients with primary hyperparathyroidism and hypertension secrete parathyroid hypertensive factor (PHF). Parathyroidectomy decreases blood pressure in these rats and in patients. The present study determined whether phPTX induced by calcimimetics decreases mean arterial blood pressure (MAP) in hypertensive rats. METHODS: Hypertensive SHR and normotensive Wistar Kyoto (WKY) rats were used. Clearance experiments were performed and the effect of 1 mg/kg body weight (given intravenously) synthesized NPS R-568 (NPS) on MAP in the presence or absence of thyroparathyroidectomy (TPTX) was monitored. RESULTS: The success phPTX and TPTX were proven by a significant decrease in plasma Ca(2+) concentration and a decrease in urinary fractional phosphate excretion (FE Pi). The administration of NPS significantly decreased blood pressure in SHR versus SHR/control: Delta(0-50 min of experiment) MAP -16.5 +/- 2.5 mm Hg v -3.2 +/- 1.5 mm Hg (P < .002). The TPTX decreased blood pressure in SHR versus SHR/control and was not different versus SHR/TPTX/NPS (DeltaMAP: -10.2 +/- 1.6 mm Hg v -3.2 +/- 1.5 mm Hg (P < .01) and v -8.3 +/- 2.2 mm Hg (P = not significant). In normotensive WKY rats application of NPS did not reach significance in DeltaMAP: -6.7 +/- 1.8 mm Hg v -2.6 +/- 2.8 mm Hg (P = not significant) in WKY/control. The TPTX lowered blood pressure in WKY versus WKY/control and remained unchanged versus WKY/TPTX/NPS (DeltaMAP: -11.3 +/- 1.7 mm Hg v -2.6 +/- 2.8 mm Hg (P < .04) and v -11.4 +/- 2.6 mm Hg (P = not significant). CONCLUSIONS: We conclude that phPTX with NPS R-568 is responsible for a decrease of MAP in SHR.

Aniline Compounds↗

PubMed2002

Regulation of renal vitamin D receptor is an important determinant of 1alpha,25-dihydroxyvitamin D(3) levels in vivo.

The synthesis of 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) is most strongly regulated by dietary calcium and the action of parathyroid hormone to increase 1alpha-hydroxylase (1alpha-OHase) and decrease 24-hydroxylase (24-OHase) in kidney proximal tubules. This study examines the hypothesis that 1,25-(OH)(2)D(3) synthesis, induced by dietary calcium restriction, is also the result of negative feedback regulation blockade. Rats fed a low calcium (0.02%, -Ca) diet and given daily oral doses of vitamin D (0, 0.5, 1.0, 2.0, 4.0, 8.0, and 16.0 microg) remained hypocalcemic despite increasing levels of serum calcium in relation to the vitamin D dose. Plasma levels of 1,25-(OH)(2)D(3) rose to high levels (1200 pg/ml) at the high vitamin D dose levels. As expected, thyroparathyroidectomy caused a rapid fall in serum 1,25-(OH)(2)D(3). In rats fed a 0.47% calcium diet (+Ca) supplemented with vitamin D (4 microg/day), exogenous 1,25-(OH)(2)D(3) suppressed renal 1alpha-OHase and stimulated the 24-OHase. In rats fed the -Ca diet, vitamin D was unable to suppress the renal 1alpha-OHase or stimulate the renal 24-OHase. In contrast, vitamin D was fully able to stimulate intestinal 24-OHase. Intestinal vitamin D receptor (VDR) was present under all circumstances, while kidney VDR was absent under hypocalcemic conditions and present under normocalcemic conditions. It appears that tissue-specific down-regulation of VDR by hypocalcemia blocks the 1,25-(OH)(2)D(3) suppression of the 1alpha-OHase and upregulation of the 24-OHase in the kidney, causing a marked accumulation of 1,25-(OH)(2)D(3) in the plasma.

Animals↗

PubMed2000

Effect of gamma-L-glutamyl-L-dopa on phosphate excretion.

gamma-L-glutamyl-L-DOPA (gludopa) is a dopamine prodrug that is relatively specific for the kidney. Because dopamine is phosphaturic, the present study compared the phosphaturic effects of the infusion of equimolar doses of gludopa (n = 8), L-DOPA (n = 8), and gamma-L-glutamyl-L-tyrosine (glutyrosine, n = 6). Glutyrosine was used as a control to evaluate the effect of the glutamyl portion of gludopa on phosphate excretion. Sprague-Dawley rats (350 to 400 g) were anesthetized with 5-sec-butylethyl-2-thyobarbituric acid (Inactin; 100 mg/kg, IP) and underwent thyroparathyroidectomy. Clearances were taken during the infusion of normal saline vehicle, followed by the infusion of gludopa, L-DOPA, or glutyrosine, all infused at the rate of 10 nmol/kg bolus and 0.8 nmol/kg/min (iv). To determine the contribution of glutamyl derivative to phosphate excretion, gludopa or L-DOPA was infused in the presence of SCH23390, a DA-1 receptor antagonist. Gludopa infusion significantly increased dopamine excretion (from 1.9+/-0.2 ng/min to 17.0+/-3.9 ng/min, delta15.0+/-3.9 ng/min, P < .008) and fractional excretion of phosphate (from 2.6%+/-0.6% to 34.8%+/-1.8%, delta32.0%+/-1.6%, P < .001). L-DOPA infusion significantly increased dopamine excretion (from 1.4+/- 0.4 ng/min to 9.7+/-1.6 ng/min, delta8.3+/-1.5 ng/min, P < .001) and fractional excretion of phosphate (from 1.7%+/-0.6% to 8.2%+/-2.0%, delta6.4%+/-1.5%, P < .004). Glutyrosine infusion significantly increased fractional excretion of phosphate (from 2.8%+/-0.8% to 17.5%+/-5.2%, delta14.6%+/-4.8%, P < .03) without changing dopamine excretion (delta0.5+/-0.2 ng/min). Infusion of gludopa in the presence of SCH23390 increased fractional excretion of phosphate (from 5.7%+/-2.5% to 12.6%+/-3.5%, delta6.8%+/-2.3%, n = 6, P < .03), whereas SCH23390 completely blocked the phosphaturic effect of L-DOPA. We conclude that gamma-L-glutamyl-L-DOPA is more phosphaturic than L-DOPA in the rat because of the combined effects of dopamine and the glutamyl moiety.

Animals↗

PubMed1976

Bicarbonate reabsorption in chronic renal failure.

Bicarbonate reabsorption was studied in dogs before and after induction of renal failure, produced by infarction of one kidney and removal of the contralateral kidney. Glomerular filtration rate and renal plasma flow decreased to 21 and 37% of control values, respectively. Fractional potassium excretion and fractional phosphate excretion increased significantly. Volume expansion resulted in a significant decrease of bicarbonate reabsorption in both control and uremic groups. At comparable levels of fractional chloride excretion, bicarbonate reabsorption was significantly higher in renal failure than in control animals. In the second group of dogs, following induction of renal failure, sodium bicarbonate was given orally in an amount sufficient to neutralize endogenous acid production. Bicarbonate reabsorption was again significantly higher than in control animals. Thyroparathyroidectomy had no effect on bicarbonate reabsorption. Absolute bicarbonate reabsorption and sodium reabsorption were lineraly related in control animals and in those in renal failure; the ratio of absolute bicarbonate reabsorption/abolute sodium reabsorption was significantly higher in renal failure than in control. These data demonstrate that renal failure is associated with enhanced bicarbonate reabsorption which is not related to the state of extracellular volume, the need to increase acid excretion or the concentrations of parathyroid hormone. These findings suggest that there are additional unknown factors controlling bicarbonate reabsorption in renal failure.

Animals↗

PubMed1978

Changes in the kinetics of muscle contraction in vitamin D-depleted rats.

Using an in situ rat soleus neuromuscular preparation, changes in the muscle contraction kinetics in response to vitamine D depletion were studied. For a single isometric contraction, the time-to-peak tension (Tp) and the time-for-recovery-half-way-to-resting tension (T1/2r) were recorded. For a 150 Hz, 300 msec tetanus, the T1/2r was determined. Animals raised on high-calcium, high-phosphate, vitamin D-depleted diets showed prolongation of all parameters. Repletion of vitamin D returned Tp and T1/2r values to normal. Neither dietary calcium deficiency nor thyroparathyroidectomy produced an prolongation of Tp or T1/2r values. Therefore, based upon the experimental data, it appears that vitamin D or one of its metabolites, independent of any effect on the serum calcium or serum phosphate concentration, is necessary for normal muscle relaxation.

Animals↗

PubMed1982

Parathyroid hormone is not anticalciuric during chronic metabolic acidosis.

The role of parathyroid hormone (PTH) on calcium excretion during chronic metabolic acidosis was investigated in intact and thyroparathyroidectomized (TPTX) acidotic and control dogs. Intact dogs fed NH4Cl for 3 days developed marked hypercalciuria as compared to intact control animals. After thyroparathyroidectomy, calcium excretion corrected per glomerular filtration rate decreased significantly in NH4Cl-treated dogs but not in the controls. This was observed in the face of a TPTX-induced fall in filtered load of calcium in both groups. After restoration of filtered load of calcium to normal by CaCl2 infusion, fractional calcium excretion at any level of fractional sodium excretion was higher in NH4Cl-treated TPTX dogs than that of TPTX controls, indicating a calciuric effect of acidosis independent of PTH. PtH (1 U/min X 60 min) was infused to examine the effect of this hormone on calcium excretion during NH4Cl-induced acidosis. In normal dogs, PTH significantly decreased absolute and fractional calcium excretion. In contrast, PTH infusion to acidotic dogs failed to decrease absolute and fractional calcium excretion. In both groups, phosphate excretion increased significantly. The higher calcium excretion of acidotic dogs during PTH infusion resulted from failure to enhance calcium reabsorption as shown by the fact that, at any level of plasma ionizable calcium, calcium excretion was higher in acidotic dogs than in controls. These findings indicate that during metabolic acidosis PTH does not exert its normal anticalciuric effect. This may contribute to the development of hypercalciuria despite PTH excess in certain clinical conditions associated with chronic metabolic acidosis.

Acidosis↗

PubMed1984

Renal phosphate excretion in spontaneously hypertensive and normotensive Wistar Kyoto rats.

Renal tubular reabsorption of phosphate was studied in unanesthetized spontaneously hypertensive (SHR) and normotensive Wistar Kyoto rats (WKY). Three-hour-urinary phosphate excretions of 12-week-old-male SHR (53.0 +/- 13.1 micrograms/mg creatinine, N = 7) and 14-week-old female SHR (81.8 +/- 12.8, N = 8) were significantly lower than those of age sex-matched WKY (12 week, 435.8 +/- 73.2, N = 8, P less than 0.01; 14 week, 423.3 +/- 75.9, N = 8, P less than 0.01). Renal clearances were performed in 14-week-old female rats after an overnight fast. The serum phosphate concentration of SHR (4.61 +/- 0.25 mg/dl) was lower than that of WKY (5.44 +/- 0.14, P less than 0.02). Urinary phosphate excretion (U Pi V = 6.85 +/- 1.83 micrograms/min) and fractional phosphate excretion (FE Pi = 13.7 +/- 2.3%) of SHR were lower than those of WKY (U Pi V = 15.9 +/- 1.87 micrograms/min, P less than 0.01, FE Pi 22.8 +/- 2.6%, P less than 0.02). Acute hyperventilation could not account for the lower excretion of phosphate in SHR, since arterial pH and PCO2 were not different between WKY and SHR. The low renal phosphate clearance of SHR was noted at a very early age; the U Pi V of 5-week-old SHR was already lower than that of WKY. Maximum tubular phosphate reabsorption (TmPi) was studied in the 12-week-old SHR and WKY after acute thyroparathyroidectomy. TmPi of SHR (241 +/- 3.0 micrograms/ml GFR/100 g, N = 7) was greater than that of WKY (204 +/- 7.0, N = 8, P less than 0.01). However, the differences in 3-hr urinary phosphate excretion and clearances of phosphate were abolished between SHR and WKY after their blood pressures were lowered by chronic hydralazine treatment. The results indicate that hypertension is responsible for the lower renal phosphate clearances in SHR.

Animals↗

PubMed1990

Factors influencing calcitriol metabolism in renal failure.

Metabolic clearance rate (MCR) and production rate (PR) of calcitriol is decreased in experimental renal failure. In this experiment, we studied uremia and secondary hyperparathyroidism as possible causes of the abnormal calcitriol metabolism. Normal rats were made uremic by infusing phosphorus-free urine for 24 hours. Both the MCR (0.22 +/- 0.01 ml/min/kg, N = 6 P less than 0.001) and the PR (16.6 +/- 1.97 ng/kg/day, P less than 0.01) of calcitriol were significantly suppressed in normal rats following urine infusion when compared to saline infused rats (MCR, 0.30 +/- 0.01; PR, 32.9 +/- 4.1, N = 6). Different levels of protein intake by rats with renal failure produced by subtotal nephrectomy also alter the PR but not the MCR of calcitriol. Thus, the synthesis of calcitriol was significantly lower in rats with renal failure fed a high protein (50% protein) diet (17.6 +/- 0.7 ng/kg/day, N = 8, P less than 0.001) than in rats with renal failure fed a normal protein (20% protein) diet (22.2 +/- 1.4, N = 7). Thyroparathyroidectomy (TPTX) did not alter the MCR of calcitriol in renal failure, even though parathyroid hormone, which may suppress the degradation enzyme, could be elevated in this model of renal failure. The MCR of TPTXed rats with renal failure (0.15 +/- 0.01 ml/min/kg, N = 7) remained lower than that of the TPTXed control rats (0.19 +/- 0.01, N = 7, P less than 0.001), and chronic infusion of PTH to TPTXed rats with renal failure did not change the MCR of calcitriol (0.15 +/- 0.01, vs. control, 0.24 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Parathyroidectomy does not prevent the renal PTH/PTHrP receptor down-regulation in uremic rats.

In a recent study we demonstrated that the PTH/PTHrP receptor (PTH-R) mRNA was markedly down-regulated in the remnant kidney of uremic rats with severe secondary hyperparathyroidism. Among the factors potentially implicated in this down-regulation, to date only PTH has been demonstrated to modulate PTH-R expression. Here, we examined the effect of thyroparathyroidectomy (TPTX) on the renal expression of PTH-R in rats with normal renal function or with chronic renal failure (CRF) induced by 5/6 nephrectomy. Four groups of rats were studied: control, TPTX, CRF, and CRF + TPTX. Moderate-degree renal failure was documented by mean (+/- SD) creatinine clearances (microliter/min/100 g body wt) of 259 +/- 40 and 212 +/- 45 in CRF and CRF + TPTX rats, compared with 646 +/- 123 and 511 +/- 156 in control and TPTX rats, respectively. Plasma phosphorus, calcitriol, and ionized calcium were significantly lower in CRF and CRF + TPTX than in control animals. Plasma ionized calcium and calcitriol were also lower in TPTX than in control rats. Plasma PTH levels (pg/ml) were increased in CRF rats (41.8 +/- 29.4), and markedly decreased in TPTX (10.1 +/- 7.8) and CRF + TPTX (8.0 +/- 3.8) rats compared with control rats (21.7 +/- 7.5). Northern blot analysis showed that the level of the steady-state PTH-R mRNA in the kidney of CRF and CRF + TPTX rats was markedly decreased compared with that of control rats, the ratios of PTH-R mRNA/beta-actin mRNA being 0.28 +/- 0.04 and 0.27 +/- 0.03 versus 0.54 +/- 0.05, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗

PubMed1977

Failure of selected endocrine organ ablation to modify the natriuresis of blood volume expansion in the dog.

1. Selected organ-ablation experiments were performed in dogs in an attempt to identify the source of the natriuretic hormone postulated to participate in the natriuresis of blood volume expansion. 2. An isolated dog kidney perfused with blood from the femoral artery of deoxycorticosterone-loaded dogs subjected to acute volume expansion with equilibrated blood served as the bioassay system for the natriuretic factor. Four groups were studied after the following procedures: group I, no ablation; group II, thyroparathyroidectomy; group III, hypophysectomy; group IV, adrenalectomy. 3. In all groups, the administration of equilibrated blood promoted a significant increase in sodium chloride excretion in the isolated kidney. The natriuresis was unrelated to changes in glomerular filtration rate, renal blood flow, renal arterial pressure, plasma protein concentration or packed cell volume. In the absence of volume expansion, sodium chloride excretion in the isolated kidney did not change or decreased. 4. These results argue against the thyroid, parathyroid, adrenal and pituitary glands as the source of natriuretic hormone.

Adrenalectomy↗

PubMed1985

Some problems associated with adenylate cyclase bioassays for parathyroid hormone.

A renal adenylate cyclase system was assessed for its suitability in the performance of parathyroid hormone (PTH) bioassays. Membrane preparations from 1 week old chicks were found to be more sensitive to PTH than material from humans, dogs or rats. Because of the presence of non-specific inhibitors and stimulators of adenylate cyclase in human serum, each serum sample was assayed in the presence and in the absence of a specific PTH inhibitor and the difference was used to calculate PTH activity. Calcium, an inhibitor of adenylate cyclase, was either removed from serum samples by pretreatment with Chelex resin or chelated during assay by means of EGTA. Human and bovine PTH (1-34) stimulated adenylate cyclase in this system to the same extent. The lower limit of detectability was 19.5 pg/ml (final concentration). The intra-assay coefficient of variation at a final concentration of 45 pg/ml was 18%. The index of precision was 0.08 +/- 0.04 (n = 7). When synthetic human PTH (1-34) was infused into three normal volunteers, the mean biological half-life of this material was found to be 3.2 min. PTH-like bioactivity could be routinely detected in sera from normal rats, while such activity was significantly decreased in rats subjected to thyroparathyroidectomy.

Adenylyl Cyclases↗

PubMed2002

Role of calcitonin in the rapid minute-to-minute regulation of plasma Ca2+ homeostasis in the rat.

BACKGROUND: Plasma ionized calcium (Ca2+) is maintained at a very stable concentration in mammals. The hormones or factors involved in the very rapid regulation of calcium homeostasis are still debated. Thus, previous results from our laboratory have clearly shown that parathyroid hormone (PTH) and 1,25(OH)2D3 are not responsible for the rapid up-regulation of plasma Ca2+ after a brief induction of hypocalcaemia. The present investigation therefore examined in vivo the possible role of calcitonin (CT) in the very rapid, minute-to-minute regulation of plasma Ca2+ in rats. STUDY DESIGN: The rapid calcaemic response to acute thyroparathyroidectomy (TPTX) and to acute selective thyroidectomy (TX) (n = 10), as well as the possible effect of CT on the very rapid recovery of plasma Ca2+ after termination of a brief induction of hypocalcaemia were studied. Hypocalcaemia was induced by a 30-min EGTA infusion in ras in three different protocols: 1 h after TPTX (n = 9) compared with control TPTX rats not given EGTA (n = 13); 1 h after TX (n = 7); and 1 h after TPTX, but during supplementation with exogenous CT (n = 8) and compared with the response in TPTX rats infused with vehicle (n = 8). RESULTS: An immediate and significant increase of plasma Ca2+ was found after TPTX (P < 0.01) as well as after selective TX (P < 0.01) in the nonfasting rats. Significant hypercalcaemia (P < 0.05) was still present in rats fasting for 2 days before these procedures, but the increase in plasma Ca2+ was considerably less (P < 0.01). After induction of a brief period of hypocalcaemia by infusion of EGTA a significant (P < 0.01) and rapid recovery of plasma Ca2+ took place within 10 min and a further increase within the next 60 min (P < 0.01), whether or not the rats were normal, TPTX, TX or were supplemented by CT during the experiments. The plasma Ca2+ recovery curves after termination of a brief induction of hypocalcaemia all had similar appearances, indicating that presence or absence of CT had no influence on this very rapid Ca2+ recovery after induction of hypocalcaemia. CONCLUSIONS: Acute removal of the tonus of CT results in an acute increase in plasma Ca2+ for up to 3 h. This effect of CT is probably mainly related to the postprandial maintenance of normocalcaemia, but is also seen in fasting rats, although to a lesser degree. The very rapid calcaemic recovery after discontinuation of a brief induction of hypocalcaemia is, however, not a result of suppressed plasma calcitonin levels.

Animals↗

PubMed2000

Chronic effect of parathyroid hormone on NHE3 expression in rat renal proximal tubules.

BACKGROUND: The most abundant Na+/H+ exchanger in the apical membrane of proximal tubules is the type 3 isoform (NHE3), and its activity is acutely inhibited by parathyroid hormone (PTH). In the present study, we investigate whether changes in protein abundance as well as in mRNA levels play a significant role in the long-term modulation of NHE3 by PTH. METHODS: Three groups of animals were compared: (1) HP: animals submitted to hyperparathyroidism by subcutaneous implantation of PTH pellets, providing threefold basal levels of this hormone (2.1 U. h-1); (2) control: sham-operated rats in which placebo pellets were implanted; (3) PTX: animals submitted to hypoparathyroidism by thyroparathyroidectomy followed by subcutaneous implantation of thyroxin pellets, which provided basal levels of thyroid hormone. After eight days, we measured bicarbonate reabsorption in renal proximal tubules by in vivo microperfusion. NHE3 activity was also measured in brush border membrane (BBM) vesicles by proton dependent uptake of 22Na. NHE3 expression was evaluated by Northern blot, Western blot and immunohistochemistry. RESULTS: Bicarbonate reabsorption in renal proximal tubules was significantly decreased in HP rats. Na+/H+ exchange activity in isolated BBM vesicles was 6400 +/- 840, 9225 +/- 505, and 12205 +/- 690 cpm. mg-1. 15 s-1 in HP, sham, and PTX groups, respectively. BBM NHE3 protein abundance decreased 39.3 +/- 8.2% in HP rats and increased 54.6 +/- 7.8% in PTX rats. Immunohistochemistry showed that expression of NHE3 protein in apical BBM was decreased in HP rats and was increased in PTX rats. Northern blot analysis of total kidney RNA showed that the abundance of NHE3 mRNA was 20.3 +/- 1.3% decreased in HP rats and 27. 7 +/- 2.1% increased in PTX. CONCLUSIONS: Our results indicate that the chronic inhibitory effect of PTH on the renal proximal tubule NHE3 is associated with changes in the expression of NHE3 mRNA levels and protein abundance.

Animals↗