Disease relevance of PTH

• The maximal PTH response to hypocalcemia was similar among the three groups [1].
• Acute alkalosis may directly affect PTH secretion [1].
• INTRODUCTION: We recently showed that acute metabolic and respiratory acidosis stimulated PTH secretion [1].
• However, the maximal PTH response was observed after a decrease in ionized calcium of 0.20 mM in the control group but not until a decrease of 0.40 mM in the metabolic and respiratory alkalosis groups [1].
• In contrast to the metabolic alkalosis group, hypernatremia (157 +/- 2 mEq/liter) in the hypertonic saline group was associated with an increased PTH value (46 +/- 4 pg/ml) [1].

Psychiatry related information on PTH

• This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations [2].

High impact information on PTH

• Parathyroid hormone: a coronary artery vasodilator [3].
• Aluminum-induced de novo bone formation in the beagle. A parathyroid hormone-dependent event [4].
• Administration of higher doses of aluminum (1.20 mg/kg) increased the serum aluminum further (1242.3 +/- 259.8 micrograms/liter) but did not affect calcium, creatinine, or parathyroid hormone [5].
• Parathyroid hormone (PTH) produced a dose-dependent immediate stimulation of inositol triphosphate and diacylglycerol production in the opossum kidney cell line, primary culture proximal tubular cells, and basolateral membranes from canine proximal tubular segments [6].
• These results demonstrate that PTH may activate renal tubular epithelial cells by the production of inositol triphosphate and diacylglycerol [6].

Chemical compound and disease context of PTH

• During the next 30 minutes, disodium EDTA was infused to induce hypocalcemia and to evaluate the PTH response to hypocalcemia [1].
• The dietary hyperparathyroidism resulted in desensitization of the PTH-responsive adenylate cyclase (Vmax 3,648 +/- 654 pmol cyclic (c)AMP/mg protein per 30 min in hyperparathyroid animals vs. 5,303 +/- 348 in normal controls) [7].
• Subsequent chelator (EGTA)-induced chronic normalization of hypercalcemia during ongoing PTH infusion resulted in a large and sustained increase in plasma calcitriol concentration to supernormal levels, reversible during subsequent cessation of chelator infusion [8].
• The present study examined the role of PTH in glucose intolerance of chronic renal failure (CRF) [9].
• Ca++ administration, but not hypophosphatemia or PTH infusion, increased significantly the mean insulin response to tolbutamide [10].

Biological context of PTH

• Perfusate from kidneys with lower glomerular filtration rates (GFR) contained b-PTH 1-84 for longer periods of time than kidneys with higher GFRs, and perfusate from kidneys with lower GFRs demonstrated greater accumulation of carboxyl terminal PTH fragments [11].
• The Kact (concentration of PTH required for half-maximal enzyme activation) was unchanged [7].
• However, the percent extraction of immunoreactive PTH was unchanged in chronic renal disease, and the observed decrease in RC was due to changes in renal plasma flow [12].
• The results of this study suggest that target cell resistance to PTH in patients with hyperparathyroidism might occur, at least in part, due to down-regulation of PTH receptors by circulating hormone [13].
• Phosphorylation of BBMV and PTH treatment in vivo had similar effects on BBMV phospholipid composition increasing the levels of anionic phospholipids [14].

Anatomical context of PTH

• After 6-9 wk on the diet the animals were killed and basolateral renal cortical membranes prepared for the study of the PTH receptor-adenylate cyclase system in vitro [7].
• To study the subcellular mechanism of this phenomenon we evaluated PTH receptors and adenylate cyclase activity in renal cortical membranes prepared before and after infusion of bovine parathyroid gland extract (PTE) into thyroparathyroidectomized dogs [13].
• The present studies were designed to examine the consequences of chronic mild elevations of endogenous parathyroid hormone (PTH) in vivo on the PTH receptor-adenylate cyclase system of canine kidney cortex [7].
• Sinus node maximum diastolic potential, activation voltage, and amplitude were unchanged by PTH or PTHrP (P>.05) [15].
• The phosphaturic action of parathyroid hormone (PTH) could be mediated through the cAMP-dependent phosphorylation of specific brush-border membrane proteins [16].

Associations of PTH with chemical compounds

• PTE infusion resulted in a 53% decrease in the number of high-affinity receptors (P less than 0.01) associated with a 66% decrease in PTH-stimulated adenylate cyclase (P less than 0.01) relative to paired base-line values [13].
• The long-term potency of plasma calcium concentration as a modulator of calcitriol metabolism is sufficient to override opposing modulation by plasma phosphorus concentration and PTH [8].
• The effect of infusing PTH on the urinary excretion of cyclic AMP (cAMP) and PO4= was examined in five normal dogs at two different levels of serum Mg++ [17].
• The data show that (a) glucose intolerance does not develop with CRF in the absence of PTH, (b) PTH does not affect metabolic clearance of insulin or tissue resistance to insulin in CRF, and (c) the normalization of metabolism in CRF in the absence of PTH is due to increased insulin secretion [9].
• Whether serum Mg++ concentrations also modify the action of PTH on its target organs has not been definitively established [17].

Physical interactions of PTH

• These studies also provide further confirmation that PTH and PTHrP bind to a structurally indistinguishable renal receptor and validate the use of PTHrP as a ligand for studies designed to characterize and purify the PTH receptor [18].

Regulatory relationships of PTH

• 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 [19].

Other interactions of PTH

• Infusion of the PTE vehicle alone did not affect PTH receptor number or blunt the adenylate cyclase response to PTH [13].
• The data are consistent with the notion that excess PTH reduces post-heparin LPL activity in plasma, which in turn results in impaired lipid removal from the circulation and consequently hyperlipidemia [20].
• These data suggest that PTH, while acting directly on the kidney to increase phosphate and sodium excretion, does not elevate renin secretion by a direct renal action [21].
• Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus [22].
• The Na+-gradient Pi overshoot in vesicles isolated from normal, GH-treated and thyroparathyroidectomized dogs was increased after in vivo PTH administration [23].

Analytical, diagnostic and therapeutic context of PTH

• Blood levels of circulating immunoreactive PTH were determined by radioimmunoassay [12].
• The half-life of intact PTH (iPTH) was determined during hypocalcemia when PTH was measured after parathyroidectomy [24].
• Re-collection micropuncture and simultaneous clearance studies were performed in thyroparathyroidectomized (TPTX) dogs to evaluate the effects of the acute administration of parathyroid hormone (PTH) on bicarbonate reabsorption [25].
• The increase in UcAMP excretion by pharmacologic amounts of PTH results from glomerular filtration of increased plasma cAMP, which may be generated in bone [26].
• Dogs were rendered deficient in 1,25-(OH)2D and PTH by five sixths nephrectomy and parathyroidectomy [27].

References