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PubMed1984

Cerebral vascular adenylate cyclase: evidence for coupling to receptors for vasoactive intestinal peptide and parathyroid hormone.

We have studied the responsiveness of vascular adenylate cyclase to vasoactive intestinal peptide (VIP) and parathyroid hormone (PTH) using preparations of cerebral microvessels and arteries. Cerebral microvessels obtained from rats, guinea-pigs, cattle, and pigs all responded potently to bovine (b) PTH-(1-34), whereas considerable between-species variability was observed in the responsiveness to VIP. The homologous peptide to VIP, PHI (porcine heptacosapeptide), stimulated adenylate cyclase in both rat microvessels and a broken-cell preparation of bovine arteries. The ED50 values for activation of bovine arterial adenylate cyclase by VIP, PHI, and bPTH-(1-34) were 6.9 nM, 10 nM, and 100 nM, respectively, with the following order of efficacy: VIP = PHI greater than bPTH-(1-34). The other related peptides, hpGRF (human pancreatic growth hormone releasing factor), secretin, and glucagon, and the fragment VIP-(10-28) were inactive. The PTH antagonist, [Nle8, Nle18, Tyr34]bPTH-(3-34) amide, inhibited bPTH-(1-34) activation of vascular adenylate cyclase but did not affect activation by VIP using either microvessels or arteries. VIP or PHI demonstrated an additive effect with bPTH-(1-34) on vascular adenylate cyclase activity. However, the effects of VIP and PHI were nonadditive with each other. These data suggest that VIP and bPTH-(1-34) activate cerebral vascular adenylate cyclase by interacting with pharmacologically distinct receptors, whereas PHI and VIP likely interact with a common receptor.

Adenylyl Cyclases↗
PubMed1998

Regulation of renal parathyroid hormone receptor expression by 1, 25-dihydroxyvitamin D3 and retinoic acid.

The renal distal convoluted tubule (DCT) is the major site of parathyroid hormone (PTH) and 1alpha,25-dihydroxyvitamin D3 [1, 25(OH)2D3]-regulated calcium absorption. 1,25(OH)2D3 augments PTH-stimulated calcium transport by DCT cells, while having no effect of its own. 1,25(OH)2D3 mediates its effects on gene expression by binding to a nuclear vitamin-D receptor (VDR), which then associates with the retinoid-X receptor (RXR) as a heterodimer. We studied the effects of 1,25(OH)2D3, 9-cis- and all-trans-retinoic acid on PTH/PTHrP receptor expression. mRNAs for the PTH/PTHrP, VDR, and RXR receptors were detected in immortalized DCT cells by reverse transcriptase-polymerase chain reaction. Changes in PTH/PTHrP receptor mRNA expression were quantified by slot blot hybridization. 1,25(OH)2D3 maximally increased PTH/PTHrP receptor mRNA levels by 70%. The stimulation was specific since 1,25(OH)2D3 treatment had no effect on the expression of adrenergic receptor or Na+/H+ exchanger mRNA levels. Likewise, the inactive form, 25(OH)2D3 had no effect on PTH/PTHrP receptor mRNA expression. In combination with the putative RXR ligand, 9-cis-retinoic acid, 1,25(OH)2D3 increased PTH/PTHrP receptor mRNA levels 4-fold. 9-cis-Retinoic acid had no effect of its own on steady-state PTH/PTHrP receptor mRNA expression. The putative ligand for the retinoic acid receptor, all-trans-retinoic acid, increased PTH/PTHrP receptor mRNA expression alone and in combination with 1,25(OH)2D3. 9-cis-Retinoic acid alone, and in combination with 1,25(OH)2D3, also increased specific PTH/PTHrP receptor binding to plasma membranes isolated from DCT cells. These results indicate that 1,25(OH)2D3 upregulated PTH/PTHrP receptor expression at both mRNA and protein levels in a manner consistent with VDR/RXR heterodimers transactivating the PTH/PTHrP receptor gene by binding a vitamin D response element in the PTH/PTHrP gene.

Alitretinoin↗
PubMed1997

Intraoperative parathyroid hormone monitoring during parathyroidectomy for secondary hyperparathyroidism.

BACKGROUND: The surgical management of secondary hyperparathyroidism by experienced surgeons is associated with excellent results. The presence of supernumerary glands and inadequate initial parathyroidectomy can lead to reoperations for recurrence. Intraoperative parathyroid hormone monitoring (qPTH), which has been described during parathyroidectomy for primary hyperparathyroidism, may be helpful in preventing or predicting the need for reoperation. This report describes the use of qPTH assays during parathyroidectomy in patients with secondary hyperparathyroidism. METHODS: Intraoperative parathyroid hormone (PTH) levels were determined in 13 patients with secondary hyperparathyroidism undergoing total parathyroidectomy with autotransplantation (n = 3) or subtotal parathyroidectomy (n = 10). Levels were determined using a modified immunochemiluminometric assay (qPTH). RESULTS: The average PTH levels before and after parathyroidectomy were 1599 pg/ml (620 to 2486 pg/ml) and 230.3 pg/ml (129 to 345 pg/ml), respectively. All patients had significant decreases in PTH levels after parathyroidectomy (mean, 84.6%). Symptoms were improved in all patients after operation. PTH levels at early follow-up were consistently below intraoperative levels. CONCLUSIONS: Intraoperative PTH monitoring reproducibly demonstrates the clinically relevant decrease in PTH levels after parathyroidectomy for secondary hyperparathyroidism similar to those previously documented in patients with primary hyperparathyroidism. Long-term follow-up and increasing numbers of patients are crucial in defining the role of qPTH monitoring during parathyroidectomy for secondary hyperparathyroidism.

Adult↗
PubMed1991

Internal ribosome-binding site directs expression of parathyroid hormone analogue (8-84) in Escherichia coli.

Expression of the human parathyroid hormone (PTH) gene in E. coli yielded intact PTH and PTH-(8-84). To determine if PTH-(8-84) is the result of a competing translation initiated from methionine codon-8 or degradation of the intact PTH, twelve new gene constructs with or without an internal ribosome-binding site (iRBS) in the PTH-(1-5) region were prepared via substitution with degenerate codons. Expression of constructs without iRBS produced only intact PTH. Constructs with weak iRBS, including one that resembles the cDNA sequence, yielded PTH-(8-84) as a minor product. In contrast, constructs with strong iRBS produced predominantly or exclusively this shorter analogue.

Binding Sites↗
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

Parathyroid hormone and bone histology: response to hypocalcemia in osteitis fibrosa.

The parathyroid hormone (PTH) response to hypocalcemia was studied in 18 hemodialysis patients with osteitis fibrosa, and the relationship with PTH and bone histology in 26 hemodialysis patients. Hypocalcemia was produced during hemodialysis by the use of a dialysate devoid of calcium. Both amino (N) (P less than 0.05) and carboxy (C) (P less than 0.005) terminal PTH attained maximum levels by 15 min despite only a minimal decline in plasma calcium. Throughout the remainder of the study, C and N-PTH levels remained elevated but did not increase despite a further decline in plasma calcium. Five patients increased both C and N-PTH to maximum or near maximum levels by the first sampling, although plasma calcium remained above 9 mg/dl. Basal C and N-PTH correlated with the maximum levels of each induced by hypocalcemia (P less than 0.005). Both basal N-PTH and the maximum change in C-PTH produced by hypocalcemia correlated with osteoblastic osteoid, active resorption, osteoclasts/mm2, and endosteal fibrosis (P less than 0.005). In conclusion, (1) a minimal decline in plasma calcium produces a maximum C and N-PTH response; (2) an altered PTH set point may be present in some hemodialysis patients; (3) the correlation between basal and maximally stimulated PTH levels suggests that basal PTH levels may reflect parathyroid gland mass; and (4) a correlation with basal and stimulated PTH and bone histology is present.

Adult↗
PubMed2002

Effects of cerivastatin and parathyroid hormone on the lumbar vertebra of aging male Sprague-Dawley rats.

Both men and women lose bone at a late age (aging bone loss). The aim of this study was to determine whether cerivastatin and parathyroid hormone (PTH) can prevent aging bone loss in men. Bone loss in aged male Sprague-Dawley (SD) rats was used as a model for age-related bone loss in men. Nine-month-old male SD rats were divided into six groups: (1) baseline controls (killed at the beginning of the study); (2) age-matched controls; (3) parathyroid hormone (PTH; 80 microg/kg body weight per day for 5 days/week) treated; (4) low-dose cerivastatin (0.2 mg/kg body weight per day) treated; and (5) medium-dose cerivastatin (0.4 mg/kg body weight per day) treated; and (6) high-dose cerivastatin (0.8 mg/kg body weight per day) treated. Groups 2-6 were treated for 23 weeks between the ages of 9 and 15 months and killed at the end of 23 weeks. The fourth lumbar vertebra was analyzed using peripheral quantitative computed tomography (pQCT). It is shown that age-matched controls had decreased cancellous bone mineral content (Cn. BMC) by 19% (p < 0.05) and cancellous bone mineral density Cn. BMD) by 22% (p < 0.01) when compared with baseline controls. All three doses of cerivastatin resulted in lower Cn. BMC and Cn. BMD when compared with age-matched controls, but this decrease was not statistically significant. In the PTH-treated group, Cn. BMC increased by 5% (p < 0.0001) and Cn. BMD increased by 37% (p < 0.0001) when compared with age-matched controls. In age-matched controls, cortical bone mineral content (Ct. BMC) and cortical bone mineral density (Ct. BMD) decreased slightly, but not significantly, when compared with baseline controls. Ct. BMD did not change significantly at any of the three doses in the cerivastatin-treated groups. In the PTH-treated group, Ct. BMC increased by 23% (p < 0.0001) when compared with age-matched controls. We confirmed that male SD rats lose bone with aging in the lumbar vertebra, and it is concluded that cerivastatin, at all doses administered, did not prevent this age-related bone loss. In contrast, PTH prevented age-related bone loss in the vertebra of male SD rats.

Aging↗
PubMed1978

Neuroendocrine modulation of calcitonin and parathyroid hormone in man.

Recent evidence suggests that of calcitonin (CT) and parathyroid hormone (PTH) is controlled by factors other than the ambient serum calcium concentration. We studied the effects of infusions of four neuroendocrine modulators upon CT and PTH levels: isoproterenol (beta-adrenergic agonist), methoxamine (alpha adrenergic agonist), prostaglandin E2, and somatostatin. Isoproterenol was a consistent secretagogue for both hormones. Maximal CT increments during isoproterenol infusion in normal subjects were 13 +/- 2 pg/ml (mean +/- SEM, n = 6, P less than 0.001; basal, 26 +/- 5). Maximal increments in PTH were 113 +/- 22 pg/ml (P less than 0.01, n = 6; basal, 430 +/- 11). Infusions of methoxamine increased CT by 13 +/- 5 pg/ml (n = 5, P less than 0.05; basal, 43 +/- 13), but had no effect on PTH. The means of the maximal CT increments during isoproterenol (21 +/- 8 pg/ml) and methoxamine infusion (28 +/- 11 pg/ml) were not statistically different from those achieved by acute elevations of serum calcium levels within the physiological range (41 +/- 23 pg/ml). Infusions of somatostatin and prostaglandin E2 had no or only transient effects on basal or stimulated CT or PTH levels. Our data suggest that adrenergic input modulates CT and PTH secretion in humans independently of changes in serum calcium.

Adult↗
PubMed1988

Photoaffinity labeling of parathyroid hormone receptors in clonal rat osteosarcoma cells.

A photoreactive derivative of a sulfur-free bovine parathyroid hormone (PTH) analogue, [Nle8,N-epsilon-(4-azido-2-nitrophenyl)Lys13,Nle18,Tyr34]bovine PTH-(1-34)-NH2 (NAP-NlePTH), was purified from the products of the reaction of [Nle8,Nle18,Tyr34]bovine PTH-(1-34)-NH2 (NlePTH) with 4-fluoro-3-nitro-phenylazide and was used to identify binding components of the PTH receptor in clonal rat osteosarcoma cells (ROS 17/2.8). The purified analogue, NAP-NlePTH, is a fully active agonist in three different ROS 17/2.8 cell bioassays: 1) specific binding to saturable PTH receptors; 2) stimulation of cyclic AMP accumulation; and 3) inhibition of cellular alkaline phosphatase activity; this analogue gave dose response curves parallel to and 25-33% as potent as its parent molecule, NlePTH. Radioiodinated NAP-NlePTH (125I-labeled NAP-NlePTH) retained maximal receptor-binding potency. Radioligand saturation studies in intact cells showed that the Kd of PTH receptors for the photoligand was slightly less than that for 125I-labeled NlePTH (2.8 and 0.8 nM, respectively), but that the Bmax was essentially identical for both radioligands (8 fmol/10(5) cells). Photoaffinity labeling of ROS 17/2.8 cells revealed several 125I-labeled macromolecular components by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. One predominant 125I-labeled band, having an apparent Mr of 80,000 daltons (including Mr = 4,347 ligand; hereafter referred to as the Mr = 80,000 protein), was consistently demonstrated in both reducing and nonreducing conditions. Its labeling was completely inhibited by coincubation with NlePTH (10 nM) at 26-fold molar excess to the photoligand, but not by biologically inactive PTH fragments or unrelated hormone. Labeling of several other macromolecular components persisted in the presence of NlePTH (1 microM). Only the labeling of the Mr = 80,000 protein showed saturation kinetics for photoaffinity labeling; the dose of 125I-labeled NAP-NlePTH (0.8 nM) to half-saturate labeling of the Mr = 80,000 protein was close to the Kd (2.8 nM) of specific binding of the photoligand to receptors in intact ROS 17/2.8 cells. Pretreatment of the cells with NlePTH and dexamethasone led to the predicted proportional decrease or increase, respectively, in labeling of the Mr = 80,000 protein. Our data, using a highly purified photoactive derivative of PTH, having carefully defined chemical and biological properties, show a plasma membrane component of Mr = 80,000 in ROS 17/2.8 cells that possesses the affinity, binding capacity, and physiological characteristics of the PTH receptor.

Affinity Labels↗
PubMed1986

Serum parathyroid hormone levels in the hypercalcaemia of urological malignant disease.

Serum parathyroid hormone (PTH) levels have been measured in 8 patients with hypercalcaemia associated with urological malignancy: 3 renal cell carcinomas, 2 adenocarcinomas of prostate, 2 transitional cell carcinomas of bladder and one transitional cell carcinoma of kidney. Five (63%) of these 8 patients had bone metastases. PTH was detectable in the serum of all 8 hypercalcaemic patients, but in only 2 cases was the PTH level above the normal range, and in one of these a coincidental parathyroid adenoma was found to be responsible for the hypercalcaemia. It appears that these tumours can produce a hormone-like substance with biological effects similar to PTH.

Aged↗
PubMed1987

The effect of an oral calcium load on plasma ionized calcium and parathyroid hormone concentrations in osteoporotic postmenopausal women.

Plasma ionized calcium (IC) and parathyroid hormone (PTH) concentrations were measured in 31 osteoporotic postmenopausal women at hourly intervals for 5 hours after a 1 g oral calcium load. Fifteen subjects had normal radiocalcium absorption and 16 subjects were malabsorbers of calcium. IC rose and PTH fell after the calcium load in both groups with a plateau at 3-4 hours, and the rise in IC was greater (P less than 0.01) in the normal absorbers. There was a nonsignificant trend for the fall in PTH to be greater in the normal absorbers. In the group as a whole the mean increase in IC (above baseline) at 4 hours was directly related to calcium absorption (P less than 0.025) and the mean change in PTH was inversely related to calcium absorption (P less than 0.05). These results demonstrate that in subjects with postmenopausal osteoporosis the responses of IC and PTH to an oral calcium load are a function of calcium absorptive status.

Administration, Oral↗
PubMed1981

Episodic secretion of parathyroid hormone in the dog.

This study was designed to determine whether parathyroid hormone (PTH) is secreted episodically, to characterize any such rhythms, and to see whether the rhythms can be altered by stimulating PTH secretion using constant hypocalcemia. We collected blood samples at 1-min intervals for 1 h from the precava or postcava of conscious dogs during normocalcemia or induced, constant hypocalcemia. In two anesthetized normocalcemic dogs we catheterized a caudal thyroid vein and collected all the effluent blood in 1-min fractions. Immunoreactive PTH (IPTH) concentrations were determined in quadruplicate, and the results were subjected to spectral analysis. In both the precava and postcava of normocalcemic dogs, there were regular oscillations in IPTH levels with a period of 12 min (range, 10-15 min) and a +/- 14% variation about the overall mean. Although significant two- to fourfold changes in IPTH levels still occurred during constant hypocalcemia, there was no significant rhythmicity. Significant cycles in IPTH concentration (mean 8.4-min period) were observed in thyroid venous effluent plasma during normocalcemia, confirming that the phenomenon represented episodic secretion that was not affected by pentobarbital anesthesia.

Animals↗
PubMed1991

Hypocalciuria of preeclampsia is independent of parathyroid hormone level.

Hypocalciuria is a feature of preeclampsia. The roles of parathyroid hormone (PTH) and vitamin D 1,25(OH)2D3 (calcitriol) in its pathogenesis have not yet been determined. Fourteen preeclamptic women were compared with 12 women with chronic hypertension and 11 normotensives, all in the third trimester. Preeclamptics had the lowest urinary calcium excretion rate (62.1 +/- 32.8 mg/24 hours) compared with chronic hypertensive women (162.6 +/- 97.8 mg/24 hours) and normotensive controls (225.6 = 146.9 mg/24 hours) (P less than .05). Serum PTH was lowest in preeclamptics (9.8 +/- 5.5 pg/mL), in contrast to the chronic hypertensives (18.5 +/- 2.7 pg/mL) and normotensives (16.4 +/- 3.2 pg/mL) (P less than .005). Similarly, urinary cyclic adenosine monophosphate (cAMP) excretion was 2.9 +/- 1.4 mumol/24 hours in the preeclamptics, 5.1 +/- 1.7 mumol/24 hours in the chronic hypertensives, and 4.6 +/- 1.3 mumol/24 hours in the normotensive group (P less than .05). These data suggest that the mechanism of hypocalciuria in preeclampsia is independent of the PTH-calcitriol axis. Therefore, it is suggested that the hypocalciuria of preeclampsia is due to intrinsic renal tubular dysfunction.

Adult↗
PubMed1995

Coordinate regulation of rat renal parathyroid hormone receptor mRNA and Na-Pi cotransporter mRNA and protein.

Parathyroid hormone (PTH) acts on the kidney by binding to the PTH receptor, leading to a decrease in the active renal reabsorption of phosphate by the Na-Pi cotransporter, which is also independently activated by hypophosphatemia. We have studied the effects of hypo- and hyperparathyroidism and hypophosphatemia on PTH receptor mRNA and Na-Pi cotransporter mRNA and protein. Both surgical parathyroidectomy and hypophosphatemia, which itself leads to hypoparathyroidism, led to an upregulation of the PTH receptor mRNA and Na-Pi cotransporter mRNA and protein. Parathyroidectomized rats fed a low-Pi diet had an increase in PTH receptor and Na-Pi cotransporter mRNAs. Diet-induced hyperparathyroidism had no effect on PTH receptor mRNA and Na-Pi cotransporter mRNA and protein. The effect of hypoparathyroidism and hypophosphatemia to increase both PTH receptor mRNA and Na-Pi cotransporter mRNA and protein shows that there is a tight coordinate regulation of these factors, which are both involved in PTH action.

Animals↗
PubMed1990

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets.

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

Animals↗
PubMed1979

Effect of parathyroid hormone on plasma renin activity and sodium excretion.

The interaction between parathyroid hormone (PTH) and the renin-angiotensin system was evaluated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH (1-34) for 1 h was accompanied by a 57% increase (13.7-21.6 ng/ml per h) in plasma renin activity (PRA) which returned toward control levels during the recovery period. Sodium and phosphate excretion also increased. Second the endogenous secretion of PTH was stimulated by infusion of citrate into the blood supply of the thyroparathyroid glands to determine if the stimulatory effect on renin occurred with endogenous secretion of PTH. Phosphate excretion increased, which confirmed PTH secretion. There was a significant rise (57%) in both PRA (6.1-9.8 ng/ml per h) and sodium excretion, the magnitude of the sodium response modulating the increase in PRA. Blood pressure remained constant. In a third set of experiments, thyrocalcitonin was infused intravenously and had no effect on PRA. These data indicate that both exogenous and endogenous PTH can elevate PRA and increase sodium excretion. The sodium effect is probably the result of inhibition of proximal sodium reabsorption by PTH. The mechanism by which PTH elevates PRA is not known.

Animals↗
PubMed1985

Actions of parathyroid hormone are not impaired during chronic metabolic acidosis.

The effect of parathyroid hormone (PTH) on renal excretion of calcium, phosphate, and bicarbonate was studied in acutely thyroparathyroidectomized dogs with metabolic acidosis. Ammonium chloride 10 gm/day for 3 days was given to 15 dogs to induce chronic metabolic acidosis. Clearance results obtained from these experiments showed that infusion of Beckman 1-34 PTH into normal and acidotic dogs resulted in a marked increase in phosphate and bicarbonate excretion, accompanied by a small reduction in calcium excretion and a slight but significant increase in plasma ultrafilterable calcium. Complementing our clearance data, micropuncture results obtained from the proximal and distal tubules of these animals indicated an enhancement of calcium reabsorption in the distal tubule after administration of PTH. Phosphate reabsorption by the proximal and distal tubules was reduced after infusion of PTH in both normal and acidotic dogs. The fraction of bicarbonate reabsorbed in the proximal tubule was reduced after PTH infusion, but the fraction of bicarbonate reabsorbed in the distal tubule remained unchanged. These data suggest that the phosphaturic, the hypocalciuric, and the bicarbonaturic effects of PTH were not impaired during chronic metabolic acidosis.

Acidosis↗
PubMed1988

Characterization of isolated and cultured chick osteoclasts: the effects of acetazolamide, calcitonin, and parathyroid hormone on acid production.

The effects of acetazolamide, calcitonin (CT), and parathyroid hormone (PTH) on acid production in isolated osteoclasts has been investigated. Osteoclasts were isolated from the endosteum of 3-week chick tibias and were maintained under culture conditions for 5 days. The cells were treated with acetazolamide (10 x 4 M and 10(-7) M), CT (1 mU/ml and 0.31 mU/ml) and PTH (6.5 U/ml and 0.40 U/ml) for 1, 3, 6, and 18 hr. The cells were stained with acridine orange and the intensity of fluorescence measured by a light microscope photometer. Acetazolamide treatment resulted in a steady decline in intracellular acidity, suggesting that carbonic anhydrase plays a major role in acid production in isolated osteoclasts. Treatment with PTH produced a decline in acidity at 1 hr, followed by a peak at 3 hr and then a decline at 6 and 18 hr. The transient increase in acidity may be due to activation of carbonic anhydrase by PTH. Calcitonin treatment also resulted in a decline in cell acidity which was similar, but less pronounced than that resulting from acetazolamide treatment. These results indicate that calcitonin may mediate osteoclast activity by alterations in intracellular acid production.

Acetazolamide↗