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PubMed1991

Effects of parathyroid hormone on urinary acidification in the rat.

To evaluate the effects of parathyroid hormone (PTH) on urinary acidification parameters, thyroparathyroidectomy was performed in normal (TPTX) and in calcium-supplemented rats (TPTX + Ca2+). Both groups were supplemented with thyroxin. Glomerular filtration rate (GFR) fell from 7.79 +/- 0.33 in the control group (C) to 4.88 +/- 0.26 ml min-1 kg-1 in TPTX, while net acid excretion fell from 5.65 +/- 0.22 in C to 3.76 +/- 0.25 mumol min-1 kg-1 in TPTX. Kinetic data of urinary acidification obtained by microperfusion techniques in proximal tubules showed that the half-time of acidification (t/2) rose from 4.75 +/- 0.24 s in C to 8.97 +/- 0.64 s in TPTX and persisted elevated in TPTX + Ca2+ (7.40 +/- 0.43 s); in the latter group, stationary pH was not significantly different from that of the control group. Bicarbonate reabsorption (JHCO3) fell from 2.18 +/- 0.15 in C to 0.823 +/- 0.082 in TPTX and was 1.53 +/- 0.073 nmol s-1 cm-2 in TPTX + CA2+. These data suggest that normal pH gradients depend on normal calcium levels, but acidification half-times are dependent on PTH, which also contributes to keeping glomerular hemodynamics and acidification rates at normal levels.

Acidosis↗
PubMed1991

Effects of thyroid status and fasting on hepatic metabolism of apolipoprotein A-I.

Metabolism of apolipoprotein (apo)A-I was studied in normal and chow-fed hyperthyroid rats, in 24-h fasted untreated male rats, and in rats after thyroparathyroidectomy (TXPTX). Rats were made hyperthyroid by administration of T3 (9.6 micrograms/day) or T4 (30 micrograms/day) with an Alzet osmotic minipump. Hyperthyroidism produced a similar two- to threefold elevation in plasma levels of apoA-I in male or female animals. During treatment with T3, plasma levels of T3 ranged from 200 to 400 ng/dl and did not correlate with plasma apoA-I levels. The net mass secretion and synthesis ([3H]leucine incorporation) of apoA-I by perfused livers from male hyperthyroid rats was elevated, while secretion of albumin was not different than that of euthyroid rats. Furthermore, the incorporation of [3H]leucine into total perfusate and hepatic protein was not altered by hyperthyroidism. The effect of thyroid hormone on apoA-I synthesis, therefore, does not appear to be a general effect on protein synthesis. After longer periods of treatment (28 days) with T3 (9.6 micrograms/day), hepatic apoA-I production decreased from that observed after 7 or 14 days of treatment, yet plasma apoA-I concentrations remained elevated. Plasma T3 decreased from 100 ng/dl to 40 ng/dl, in the hypothyroid rat resulting from TXPTX, but the plasma concentration of apoA-I did not change during the 2-week experimental period. The net secretion of apoA-I by livers from hypothyroid animals was depressed and albumin was uneffected compared to the euthyroid. Overnight fasting of euthyroid rats did not alter hepatic apoA-I secretion or plasma apoA-I levels, although under fasting conditions we had reported that hepatic output of apoB and E of VLDL is depressed. The addition of oleic acid to the perfusion medium, sufficient to stimulate VLDL production, did not affect net hepatic secretion of apoA-I by livers from euthyroid, hyperthyroid, or hypothyroid rats. In summary, hepatic synthesis of apoA-I appears to be controlled independently of other apo-lipoproteins and secretory proteins (albumin). Hepatic apoA-I synthesis is sensitive to thyroid status, increased in the hyperthyroid and decreased in the hypothyroid state. The specific stimulation of hepatic synthesis and secretion of apoA-I in the hyperthyroid state, however, tends to normalize over an extended period, perhaps from compensatory effects of a hormonal nature.

Animals↗
PubMed1978

Action of parathyroid hormone, with special reference to its anabolic effect on different kinds of tissues in rats (I).

The effect of parathyroid hormone (PTH) on the spongiosa of the proximal tibia and the alveolar bone in immature rats was studied using a time marker by the injection of lead acetate. 1) When intact rats were fed on a low calcium diet, the promotion of the apposition of the alveolar bone and the longitudinal formation as well as the resorption of the spongiosa were observed, but no change was detected in the serum calcium level. The resorption was more remarkable than the formation. 2) By parathyroidectomy (PTX) or thyroparathyroidectomy (TPTX) the effect described in 1) disappeared completely, but there subsequently occurred a fall of the serum calcium level and a marked inhibition of the formation and resorption. The decrease in the appositional formation was stronger than in the longitudinal formation. 3) When PTH was injected into the rats having undergone PTX or TPTX, all of the effects in 2) were reversed with the recovery of the apposition being at an extremely high rate. All the foregoing results indicate that PTH has an evident anabolic action in addition to the action of increasing the bone resorption and that the sensitivity to PTH is stronger in the periosteal bone than in the spongiosa.

Alveolar Process↗
PubMed1986

Differential biological effects of calcitonin and parathyroid hormone on isolated perfused bone.

These studies examine the release of 3',5'-cyclic adenosine monophosphate (cyclic AMP) from isolated perfused canine bones in response to synthetic bovine parathyroid hormone (syn b-PTH 1-34) and human calcitonin (hCT). Bones for perfusion were obtained from three groups of dogs: control (n = 11); thyroparathyroidectomized (n = 7), and mithramycin-treated thyroparathyroidectomized animals (n = 5). The results indicate that PTH causes a greater release of cyclic AMP from adult bones than CT; the addition of the two hormones simultaneously results in a synergistic rather than an additive effect; mithramycin inhibits the cyclic AMP response to calcitonin; and thyroparathyroidectomy decreases the cyclic AMP release in response to CT stimulation, suggesting that the cells (osteoclast-like) that respond to CT have an impaired response in the absence of PTH; acute TPTX does not affect the response of the cell populations of adult bones to PTH.

Animals↗
PubMed1986

Altered vitamin D metabolism in the spontaneously hypertensive rat.

To test the possible impairment of vitamin D metabolism in hypertension, we studied the effect of parathyroid hormone (PTH) on the renal production of 1,25-dihydroxyvitamin D [1,25(OH)2D] in spontaneously hypertensive rats (SHR) before (at 4 weeks of age) and after (at 12 weeks of age) the onset of hypertension. Basal serum of 1,25(OH)2D was normal in SHR at both ages. At 4 weeks of age, rise in serum 1,25(OH)2D following PTH injection (50 U subcutaneously every 2 h, four times) was also normal in SHR. By contrast, at 12 weeks of age it was approximately one-third of that in Wistar-Kyoto rats (WKY) in parallel with an attenuated response to PTH of renal production of 1,25(OH)2D. Basal 1,25(OH)2D production by the kidney in SHR was higher than that in WKY at both ages, which was abolished by thyroparathyroidectomy but not by parathyroidectomy. These data demonstrate that altered vitamin D metabolism exists even before the onset of hypertension in SHR.

Animals↗
PubMed1978

[Caryometric studies on the cortex of the adrenal gland of parathyroidectomized and thyroparathyroidectomized female rats both during and without hormonal substitution (author's transl)].

80 female Wistar rats were either parathyroidectomized or thyroparathyroidectomized and subsequently substituted with one of the following hormone regimes: thyroxine, parathormone, calcitonin, thyroxine + parathormone, or thyroxine + calcitonin. On the fifteenth day following the operation the animals were killed, the adrenals immediately removed, fixed in Bouin's fluid, dehydrated through methylbenzoate and embedded in paraffin. 5 micrometer thick sections were stained with hematoxylin--Organe G--phosphotumgstic acid--Aniline blue (HOPA). From 5 different animals in each experimental group, 200 nuclear diameters were measured in the Zona glomerulosa, Z. Fasciculata, and Z. reticularis. Statistically significant differences (P less than 0.01) were found only in those cases were the hormonal balance between thyroxine, parathormone and calcitonin was disturbed, i.e. in experimental groups receiving one of the above mentioned hormonal regimes following operation. In contrast, no significant difference was attained in nuclear diameter between nonoperated animals and those animals in which all three hormones were lacking, i.e. when a thyroparathyroidectomy was performed.

Adrenal Cortex↗
PubMed1978

Hypocalcemic effect of phentolamine.

The effects of phentolamine on calcium and phosphate metabolism were studied in young female rats. The i.p. administration of phentolamine (1.3 to 35.1 mg/kg) produces hypocalcemic and hypophosphatemic responses that resemble those produced by the hormone calcitonin. The hypocalcemic response to phentolamine reaches a maximum one hour post injection and blood calcium concentrations return to normal three hours following drug administration. Bilateral nephrectomy does not negate the hypocalcemic effect of phentolamine indicating that the drug effect is not mediated by increased renal excretion of calcium. Thyroparathyroidectomy inhibits the hypocalcemic activity of phentolamine. The mechanism of action of phentolamine with respect to changes in circulating calcium does not involve alpha adrenergic receptor blockage since large doses of tolazoline do not result in alterations in the plasma concentration of calcium. Labeling experiments with 45Ca indicate that the administration of phentolamine results in an inhibition of bone resorption.

Animals↗
PubMed1983

Graded nephron mass reduction and renal synthesis of 1,25-dihydroxyvitamin D3 in the rat.

The effect of graded nephron mass reduction by partial nephrectomy and the influence of parathyroid hormone and dietary phosphorus (P) on the production of 1,25-dihydroxy-vitamin D [1,25(OH)2D] were studied in vitamin D deficient rats. At 48 hours (acute experiments) or 2 weeks (chronic experiment) after partial nephrectomy, the rates of [3H]1,25(OH)2D production from [3H]25 hydroxyvitamin D (25-OHD) were measured in vivo. The production of 1,25(OH)2D decreased in proportion to the remaining nephron mass, and it was not greater in chronic experiments than in acute experiments at any level of nephron mass reduction. By contrast, plasma creatinine was elevated in 5 of 6 nephrectomized rats in acute, but not in chronic, experiments, suggesting the compensatory mechanism for renal excretory function but not for 1,25(OH)2D production. Further, at any level of nephron mass reduction, the production of this active metabolite was not greater in rats fed low P diet than those fed normal or high P diets. Thyroparathyroidectomy at 12 hours prior to a dose of [3H]-25)OHD suppressed 1,25(OH)2D production at any level of nephron mass reduction in rats fed normal or high P diet. These data suggest that in both experimental acute and chronic renal failure 1,25(OH)2D production is proportional to residual nephron mass and that parathyroid hormone may enhance the metabolism of 25OHD in renal failure and also may be critical for 1,25(OH)2D in normal or high P diet.

Animals↗
PubMed1982

[The influence of maternal calcitonin on fetal plasma calcium in the rat (author's transl)].

The relative fetal autonomy for plasma calcium in regard to the maternal plasma value led us to investigate a possible effect of maternal hormones on the placental transfer of calcium. For this purpose we have used pregnant Rats deprived of endogenous calcitonin (CT) by thyroidectomy (TX) or thyroparathyroidectomy (TPTX). Increases in fetal plasma calcium of 0.87 mg/dl for TX mothers, 2.46 mg/dl for TPTX mothers, and 0.54 mg/dl for normal mothers occurred at the end of a 1 hr. maternal calcium infusion 3.6 mg/100 g body weight) at 21.5 days of gestation. The absence of CT in TX and TPTX mothers and the already known reduced levels of placental Calcium-binding protein (CaBP) in TPTX Rats might explain these results. Maternal CT seems to have an inhibitory effect on the placental transfer of calcium, whereas placental CaBP might play a more important role as a "buffer".

Animals↗
PubMed1978

Hypercalcemia secondary to chronic renal failure in the dog: a report of four cases.

Hypercalcemia occurred in 4 dogs with renal failure. Primary causes of hypercalcemia previously described in the dog (primary hyperparathyroidism, pseudohyperparathyroidism, vitamin D toxicosis) were not identified. Increased concentrations of circulating immunoreactive parathormone were found in 2 dogs, and thyroparathyroidectomy of 1 dog resulted in decreased serum concentrations of that hormone as well as of calcium. The latter observations indicated that hypercalcemia was related to increased parathormone activity, but the possibility of other homeostatic imbalances was not excluded. It was concluded that renal failure should be considered as a primary cause of hypercalcemia, along with other causes previously identified.

Animals↗
PubMed1980

Modification of lethality induced by staphylococcal enterotoxin B in Dutch rabbits.

Intramuscular injection of staphylococcal enterotoxin B (SEB) at a dosage level of 50 microgram/kg of body weight caused death in Dutch rabbits. Lethality was not modified markedly by morphine pretreatment or by hyperthermia, thyrotoxicosis, propylthiouracil feeding, thyroparathyroidectomy, water deprivation, or fasting. The administration of acetylsalicylic acid to the SEB-inoculated rabbit also failed to protect the rabbits from the effect of SEB. Seemingly, the SEB molecular destruction was not markedly modified by alteration of cellular metabolism, and lethal effects of SEB remained unchanged in the morphine- or acetylsalicylic acid-treated rabbits. When SEB was given to six rabbits 3 days after total-body X-irradiation, fever persisted and three rabbits survived. An identical dose of SEB to nonirradiated rabbits produced fever initially, followed by hypothermia and death of all six rabbits.

Animals↗
PubMed1980

Adrenal regeneration hypertension prevented by thyroidectomy: a quantitative ultrastructural study of the regenerating adrenal cortex.

Thyroparathyroidectomy (TPX) prevents adrenal regeneration hypertension (ARH) in female rats and concomitantly inhibits regeneration of the adrenal cortex. Removal of the thyroid gland plays the major role in preventing ARH inasmuch as parathyroidectomized adrenal-enucleated (PX-AE) rats became hypertensive, whereas thyroparathyroidectomized adrenal-enucleated rats (TPX-AE + PT) did not. Inhibition of adrenocortical regneration by TPX is reflected by a significant decrease in adrenal weight, volume of cortical parenchymal tissue per gland, and average cell volume at three weeks, compared with the regenerating adrenal gland in adrenal-enucleated thyroid-parathyroid-intact (AE) rats. Mitochondria in TPX-AE rats resembled closely those from zona fasciculata cells of a normal adrenal gland; stereologic techniques for electron microscopic examination confirmed that mitochondrial volume/cell and surface area of total mitochondrial membranes/cell (outer/inner membranes plus cristae) of adrenocortical cells from TPX-AE rats did not differ significantly from those of AE animals. The surface area of mitochondrial cristae of TPX-AE rats, however, was significantly greater than that of AE rats, whereas the surface area of the inner/outer mitochondrial membrane of the TPX-AE group was decreased significantly as compared with that of the AE group. The diameter of mitochondria in TPX-AE rats was larger than in the AE group, although the number of mitochondria/cell was significantly less in TPX-AE rats than in AE rats. Although TPX had no significant effect on the levels of DOC or corticosterone in the serum of quiescent AE rats as compared with TPX-AE rats, the rise in DOC in the serum after ether stress was blunted in the TPX-AE group as compared with that in the AE group. The rise in corticosterone in the TPX-AE group was comparable to that of the AE animals. Thus, partial inhibition of adrenal regeneration in TPX-AE rats in combination with a blunted rise in DOC levels in response to stress may well contribute to the prevention of ARH.

Adrenal Cortex↗
PubMed1980

Influence of non-steroidal anti-inflammatory compounds on the hepatic tryptophan pyrrolase activity in hypo- and hyperthyroid rats.

Hypothyroid state induced in the rat by thyroparathyroidectomy does not modify the activity of hepatic tryptophan pyrrolase (TPO) while hyperthyroidism, obtained after daily injection of 3, 3', 5-triiodo-L-thyronine, inhibits significantly the liver TPO activity. Treatment with oxametacine, indomethacin, phenylbutazone, flufenamic acid and acetylsalicylic acid, increases the activity of hepatic TPO in hypothyroid state, whereas, in hyperthyroid rats, the same drugs are able to restore the normal enzymatic activity, except for acetylsalicylic acid. During the development of an acute inflammatory process, provoked by carrageenan injection, the treatment with non-steroidal anti-inflammatory agents induces an enhancement of hepatic TPO activity. On the contrary, such enzymatic activity appears unaffected in chronic inflammation induced by cotton-pellet implantation.

Animals↗
PubMed1980

[Additive phosphaturic action of parathyrin and calcitonin (author's transl)].

Parathyrin and calcitonin exert their effects on phosphate metabolism by influencing the functions of at least three organ systems, i. e. bone, gut and kidneys. To study the renal effects of these hormones under exclusion of systemic effects microinfusion studies were performed in anesthetised rats. After thyroparathyroidectomy radioactively labelled phosphate containing solutions were microinfused into single proximal convoluted tubules. The tracer recovery in the urine allowed calculation of phosphate reabsorption in the nephron segments beyond the micropuncture site. After a control period of 6 minutes the hormones were superfused to the nephron surface and tracer recovery measured during the following 36 minutes. Within few minutes both, parathyrin and calcitonin, clearly reduced phosphate reabsorption. Infusions of supramaximal doses of either hormone abolished the local action of this hormone but did not influence the effect of the other. Thus the phosphaturic actions of parathyrin and calcitonin are additive, indicating that the hormones involve different mechanisms and/or nephron sites.

Animals↗
PubMed1995

Role of dopamine in the exaggerated phosphaturic response to parathyroid hormone in the remnant kidney.

The remnant kidney (RK) exhibits an exaggerated phosphaturic response to parathyroid hormone (PTH) infusion. Increased urinary dopamine synthesis per nephron has been demonstrated in the remnant kidney, and dopamine infusion is phosphaturic. Therefore, the role of dopamine in the exaggerated phosphaturic response to PTH infusion in the RK was evaluated. To obtain the RK model, Sprague-Dawley rats were anesthetized and subjected to right nephrectomy as well as surgical ablation of the left renal poles. Sham surgery was performed in the other groups of rats. Four weeks later, acute experiments were performed in these animals. Two hours after thyroparathyroidectomy, a control clearance was taken. Subsequently, PTH (33 U/kg bolus, 1 U/kg/min) was infused for 60 minutes, followed by a 30-minute experimental clearance. In the rats with an RK, the increase in the fractional excretion of phosphate (FEPi) in response to PTH infusion was (delta 38.5% +/- 4.2%, n = 12). In an additional group of rats with an RK, the specific DA-1 receptor antagonist (SCH 23390, 25 micrograms/kg/min) was infused for 30 minutes, a control clearance was taken, and then PTH was infused. Infusion of SCH 23390 significantly blunted the phosphaturic response to PTH (FEPi, delta 24.0% +/- 7.7%, n = 7). In contrast, the phosphaturic response to PTH was similar in the rats that underwent sham surgery in the presence (delta FEPi, 25.4% +/- 1.6%, n = 5) and absence of infusion of SCH 23390 (delta FEPi 24.7 +/- 3.1%, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Selective parathyroidectomy of the dog.

Selective parathyroidectomy (PTX) is preferred to thyroparathyroidectomy (TPTX) when specific effects of parathyroid hormone depletion are being studied. However, because of the anatomic proximity of thyroid and parathyroid glands, TPTX often is performed, leaving animals depleted of thyroxine (T4) and calcitonin as well as parathyroid hormone (PTH). In the present study, six normal dogs had parathyroid tissue and about seven-eighths of thyroid tissue removed. This quantity of thyroid tissue was inadequate to maintain normal serum T4 concentrations, despite allowance of 168 days for thyroid recovery. Five of six dogs with reduced renal mass had successful selective PTX and normal serum T4 concentrations at 28 days, when one-half or more of thyroid tissue was spared. We conclude that with attention to the surgical technique, selective PTX can be achieved in a high percentage of dogs and sufficient thyroid tissue spared to maintain euthyroidism.

Animals↗
PubMed1977

Effects of volume expansion and parathyroid hormone on total renal blood flow and its intracortical distribution.

Clearance and renal blood flow studies were performed during hydropenia, 2.5 and 10 percent steady-state saline expansion, and acute administration of parathyroid hormone (PTH) in chronically thyroparathyroidectomized (TPTX) dogs and during hydropenia and 10 percent expansion in intact dogs. Renal cortical blood flow distribution was measured with radioactive microspheres In TPTX dogs, 2.5 percent expansion increased sodium excretion but did not alter total or intracortical blood flow. With 10 percent expansion, sodium excretion and juxtamedullary (zone 4) blood flow increased in both TPTX and intact dogs. There was no correlation between the changes in sodium excretion and zone 4 fractional blood flow in either group. Although the acute administration of PTH to TPTX dogs did not alter total or intracortical blood flow, control period hemodynamic data revealed an inner shift of flow in TPTX as compated to intact dogs.These results indicate that (1) massive (10 percent), but not mild (2.5 percent), volume expansion produces an inner shift of cortical blood flow; (2) this shift does not correlate with sodium excretion, nor is it influenced by thyroparathyroidectomy: and (3) PTH does not acutely alter renal blood flow distribution, but its chronic absence is associated with a shift of flow to the inner cortex.

Animals↗