350 Parathyroid Hormone and the Placental Barrier

Krukowski, Marilyn; Lehr, David

doi:10.1016/0006-2952(61)90532-9

Cited by 7 publications

(12 citation statements)

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“…These findings are consistent with calcium-sensing receptors that determine the fetal blood calcium level, as opposed to the fetal blood calcium being determined by active placental calcium transport. Moreover, acute alterations in the maternal blood calcium of rodents and primates (such as by infusions of calcium, calcitriol, calcitonin, PTH, or EDTA) had minimal or no effect on the fetal blood calcium level (87,214,345,478,547). However, although a high fetal blood calcium level was maintained in fetal rats between the 12th and 17th days of gestation after maternal parathyroidectomy, it declined during the last several days of gestation, the interval when the skeleton is most rapidly accreting mineral (106,208,220).…”

Section: Animal Datamentioning

confidence: 99%

“…PTH circulates at lower levels in the fetal circulation compared with the maternal value in rodents, lambs, and calves (118,623,675,685,715). These low values likely derive from the fetal sources because intact PTH does not cross the placenta of non-human primates, sheep, and rodents (196,205,341,345,478). The fetal parathyroids begin to express PTH by mid-gestation in rats and lambs (390,602), and must be its dominant source because genetic ablation of the parathyroids (in Hoxa3 null fetal mice) results in undetectable serum PTH (336,341).…”

Section: Pthmentioning

confidence: 99%

“…Full-length PTHrP has about twice the molecular weight of PTH, and since PTH does not cross the placenta (196,205,341,345,478), full-length PTHrP is also unlikely to cross.…”

Section: Pthrpmentioning

confidence: 99%

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Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

207

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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Section: Animal Datamentioning

confidence: 99%

Section: Pthmentioning

confidence: 99%

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Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

207

188

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“…Calcium homeostasis has been much studied in the adult mammal, and there is an extensive literature which agrees that during late foetal life foetal total plasma calcium is greater than that of the mother [Rat: Krukowski and Lehr, 1963;Jost et al, 1963;dog: Hoskins andSnyder, 1927-8 and1933;monkey: MacDonald et al, 1965;cow: Robinson and Huffman, 1926;Plumlee et al, 1952;sheep: Bawden et al, 1965;guinea pig: Burnette et al, 1968;and man: Smith, 1951]. In some cases, differences of as much as 5 mg/100 ml.…”

mentioning

confidence: 99%

“…protein concentration [McLean and Hastings, 1935] and blood pH [Collip, 1927;Krukowski and Lehr, 1963], and of a factor which might be expected to influence the foetal plasma calcium level, namely the calcification of the foetal skeleton.…”

mentioning

confidence: 99%

Calcium Homeostasis in the Foetal Guinea Pig

Graham

Scothorne

1970

Exp Physiol

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Plasma total calcium levels have been studied in pregnant guinea pigs and their foetuses from 26 days of gestation to term. Between 28 days and 33-39 days the foetal plasma calcium falls from nearly the maternal level (9.6 mg/100 ml.) to 5-5 mg/100 ml. Thereafter the foetal plasma calcium rises, reaching the maternal level at term. No trend is found in the maternal levels. Foetal skeletal ossification was studied using an alizarin stain technique. Ossification centres appeared first in the clavicle, face and skull at 26 days of gestation. After 27 days gestation (foetal plasma protein = 1 g/100 ml.) there is a steady rise in foetal plasma protein level and at term foetal and maternal levels are approximately equal. Between 41 days gestation and term foetal blood is consistently more acid than maternal blood and has a higher pCO2 and lower P02. There is no evidence of a progressive change during gestation in pH, P02 or pCO2 in either foetal or maternal blood. It is concluded that the fall in foetal plasma calcium between 28 days and 33-39 days gestation may be due to calcification of the foetal skeleton before the full establishment of calcium homeostasis in the foetus. Increasing foetal plasma protein concentration or foetal parathyroid activity may account for the rise in foetal plasma calcium after 33-39 days.

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Fetal‐maternal Plasma Calcium Relationships in the Rabbit

Graham

Porter

1971

Exp Physiol

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Plasma total calcium levels have been studied in pregnant rabbits and their fetuses from 16 days gestation to term. Between 16 and 21 days gestation the observed fetal plasma calcium level falls from the maternal level or above to 1-6 mg/100 ml. below the maternal level. Thereafter, the fetal plasma calcium rises and at 30 days gestation exceeds the maternal level by 1*9 mg/100 ml. There is a high correlation between fetal and maternal levels at 21 days which is lost by 30 days. Fetal skeletal calcification was studied using an alizarin stain technique. The earliest centres of calcification were present in the clavicle and mandible at 16 days. It is concluded that the observed fall in fetal plasma calcium near mid-gestation may be due to the onset of skeletal calcification and the increase after 21 days to one or more of a variety of factors. Five 21 days pregnant animals were infused with 1 per cent calcium chloride solution (1 g anhydrous calcium chloride in 100 g aqueous solution) for up to 2j hr. The maternal plasma calcium concentration was elevated by 7.7 mg/100 ml. during the infusion but the fetal level was only raised by 2-0 mg/100 ml. The correlation between fetal and maternal levels was lost during the infusion. These findings are compatible with either slow calcium transfer across the placenta or fetal calcium homeostasis. It is well established in many mammalian species that during late gestation there is a greater concentration of calcium in fetal than in maternal plasma. In the guinea pig, on the contrary the fetal plasma calcium concentration at mid-gestation falls from about the maternal level (9.6 mg/100 ml.) to 5-5 mg/100 ml. and then slowly rises, reaching the maternal level again only near the end of gestation [Graham and Scothorne, 1970]. This paper presents a study of maternal and fetal levels, from a relatively early stage in gestation, in another species. The rabbit was chosen since there is already some evidence that fetal levels are lower than maternal at 21-23 days of gestation [McIsaac, 1927; Economou-Mavrou and McCance, 1958]. The stage in gestation when the homeostatic mechanism for calcium becomes mature in the fetus has not yet been identified, although there is experimental evidence that the parathyroid can elaborate hormone early in embryonic development [Scothorne, 1964: Graham and Scothorne, 1971]. In late gestation, when fetal calcium levels are higher than maternal, the fetal level remains constant when the level in the mother is elevated by infusion of calcium chloride [Bawden and Wolkoff, 1967: Greeson et al., 1968]. In this work, when low fetal levels earlier in gestation were substantiated, it was decided to study these levels after induction of maternal hypercalcaemia. METHODS The accuracy of the calcium estimation was assessed by preparing nine separate 5 ml. plasma solutions [Fawcett and Wynn, 1961] each containing 0 05 ml. of the same human plasma. The calcium content of each small sample of plasma was determined 160

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350 Parathyroid Hormone and the Placental Barrier

Cited by 7 publications

References 0 publications

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Calcium Homeostasis in the Foetal Guinea Pig

Fetal‐maternal Plasma Calcium Relationships in the Rabbit

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