Role of Adrenergic Stimuli in Parathyroid Hormone Secretion in Man

Kukreja, Subhash C.; Hargis, G. K.; Bowser, E. N.; Henderson, W. J.; Fisherman, Elmer W.; Williams, George C.

doi:10.1210/jcem-40-3-478

Cited by 133 publications

(61 citation statements)

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“…Fischer et al (18) have recently demonstrated that PTH release can be induced in cows by the infusion of epinephrine, and that this effect is mediated through a , 8 adrenergic receptor mechanism. Similar results have been obtained in human subjects (24). Also, it is well established that the parathyroid glands are encanvassed by a dense network of sympathetic nerve fibers (1, 51).…”

Section: Discussionsupporting

confidence: 85%

Parathormone and Perinatal Calcium Homeostasis

et al. 1979

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Summawand Rudd (49) have observed mean PTH concentrations in cord Plasma measured the first parathormone (PTH) and calcium concentrations were in 309 specimens collected from 190 newborns during 7 days of life. The patient material consisted of 51 preterm, 130 term, and 9 postterm infants, including 22 infants of diabetic mothers (IDM), 38 infants with hypocalcemia, and 25 asphyxiated infants. PTH was detectable, although in low concentrations, in cord blood samples despite the presence of elevated calcium concentrations. Postpartum, PTH concentrations in term, appropriate for gestational age (AGA) infants remained low during the first 2 days of life; a significant ( P < 0.05) and sustained increase in plasma hormone levels was noted starting on day 3. PTH concentrations in IDM and preterm infants remained low for 3 days and a significant hormone increase did not occur until day 4.Hypocalcemia was common in IDM and asphyxiated infants; these infants accounted for two-thirds of all hypocalcemic infants. The profde of plasma calcium in IDM during the fust week of life was different than that of any other group of infants. Plasma calcium concentrations remained depressed over this period of time and exhibited a temporary drop on day 4 accompanied by an increase in plasma PTH levels. Asphyxiated infants exhibited low plasma calcium concentrations, despite PTH levels that were significantly ( P < 0.007) higher than those of age-matched term AGA newborns. SpeculationBasal PTH secretion is present at birth, several days before the parathyroid glands appearto become responsive to hypocalcemia. Furthermore, in cord blood PTH is detectable in spite of elevated calcium concentrations. The present observatiois suggest that nonsuppressible PTH secretion, previously described in short-term animal ex~eriments. also occurs in the human fetus ex~osed to long-standing intrauterine hypercalcemia, with the implication that PTH secretion in man may be regulated by control mechanisms in addition to calcium feedback. There is anatomical and pharmacologic evidence to implicate the autonomic nervous system in this control.Hypocalcemia is a frequent problem in early postnatal Life (1 1, 20, 37, 47). Between 1970 and 1971,44 of 1390 newborns (3.2%) delivered at Harbor General Hospital, UCLA, presented with socalled "first day hypocalcemia" defmed as serum calcium levels of 5 7 mg/dl during the first 36-48 hr of life (32). Two-thirds of these infants were premature (gestation less than 38 weeks). The etiology of first day hypocalcemia remains unclear. A number of authors (17,19,46) (1 17 k 17), but were unable to detect any correlation between serum-ionized calcium on the one hand and PTH levels on the other in either maternal, cord, or infant blood between birth and age 7 days. David and Anast (13) reported similar results, yet they did observe an increase in plasma PTH in 23 of 36 infants beyond age 48 hr, and this increase correlated with a gradual rise of the low neonatal calcium concentrations toward normal. Finally, there are conflic...

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Section: Discussionsupporting

confidence: 85%

Parathormone and Perinatal Calcium Homeostasis

et al. 1979

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“…In addition, it is known that PTH synthesis is also stimulated by b adrenergic agonists and though we cannot rule out such a mechanism, it has been pointed out that this is a minor effect physiologically compared the effect produced by ionized calcium [23].…”

Section: Discussionmentioning

confidence: 85%

“…It can be speculated that parathyroid hormone (PTH) which has a more direct effect on level of ionized calcium is also perturbed by elevated lead levels [23]. It indicates that lead is an endocrine modulator and can thus be responsible for endocrinal disturbances.…”

Section: Discussionmentioning

confidence: 99%

Status of Serum Calcium, Vitamin D and Parathyroid Hormone and Hematological Indices Among Lead Exposed Jewelry Workers in Dhaka, Bangladesh

2016

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Jewelry utilizes lead either directly or as a base metal. Costume jewelry requires lead before molding and plating the product with valuable metals. Therefore, such ornaments have a great potential to release heavy metals having health hazards. Also, jewelry makers engaged in preparing German silver, an alloy, apply lead in smelting, alloying, rolling and milling silver wires and pieces. The metal is taken up by blood, soft tissues and bone. The biological effects of lead are dependent upon the level and duration of exposure. Lead inhibits three enzymes of heme biosynthesis-d-amino-levulinic-acid dehydratase (ALAD), coproporphyrin oxidase, and ferrochelatase, impairing heme synthesis and depressing serum level of erythropoietin resulting in decreased hemoglobin synthesis. Lead exposure also affects calcium metabolism and impair the synthesis of Calcitriol. In the present study, jewelry makers from Dhaka, Bangladesh, were shown to have significantly high levels of lead, protein, albumin, and parathormone in their blood, and significantly high amount of zinc-protoporphyrin and d-amino-levulinic-acid in their urine. The control group, on the other hand showed significantly higher amounts of calcium (both total and ionized form) Vitamin D 3 and non-activated erythrocyte ALAD in their blood, along with hemoglobin. It might be due to inhibition of 1-a-hydroxylase enzyme in renal tubules. Lead causes nephro-toxicity and inhibits 1-a-hydroxylase enzyme leading to decreased calcitriol synthesis resulting in impaired calcium absorption across gastro-intestinal tract and renal tubules. Low Vitamin D 3 and significantly increased Parathyroid hormone (PTH) in study group has been found.

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“…It has previously been reported that catecholamines stimulate CT and PTH secretion both in rats (Hsu & Cooper 1975) and humans (Vora et at. 1978, Kukreja et al 1975), possibly through activation of adrenergic p2 receptors (Fournier et al 1979). As secretion of catecholamines increases following trauma (Kiyomi & Brooks 1974), this may have influenced both the CT and PTH secretion in the present study.…”

Section: Discussionmentioning

confidence: 99%