Regulation of calcium homeostasis in the fetal and neonatal rat

1981 ◽  
Vol 240 (4) ◽  
pp. E367-E372 ◽  
Author(s):  
M. L. Thomas ◽  
C. S. Anast ◽  
L. R. Forte
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Mean Value ◽  
Neonatal Rat ◽  
Neonatal Rats ◽  
Newborn Rats ◽  
Circulating Levels ◽  
Immunoreactive Parathyroid Hormone

Circulating levels of calcium (Ca) and immunoreactive parathyroid hormone (IPTH), and the renal cyclic AMP responses to PTH, calcitonin (CT), and vasopressin (VP) were measured in fetal and neonatal rats. Serum Ca increased from a mean value of 9.1 mg/dl on the 19th day of gestation to 10.9 on day 20. Circulating IPTH decreased from 875 pg/ml to 213. Serum Ca declined rapidly after birth to a nadir of 7.6 by 3 h and IPTH increased to 2,006 pg/ml, indicating that fetal and newborn parathyroids are capable of responding appropriately to changes in circulating Ca. Renal responsiveness to hormones was assessed in vitro in the presence of methylisobutylxanthine, a phosphodiesterase inhibitor. The tissue cyclic AMP response to PTH and CT (15- to 18-fold over basal) was greatest at gestational days 18 and 19, progressively declined throughout the remainder of gestation, and remained low during the first 24 h after birth (6- to 7-fold). Renal cyclic AMP response to VP remained consistently low throughout this period. The depressed renal cyclic AMP response to PTH at the time of birth may contribute to the hypocalcemia found in newborn rats.

Cytochemical Evidence for Presynatic β-Adrenergic Regulation of Secretion in the Developing Rat Submandibular Gland

1977 ◽  
Vol 35 ◽  
pp. 430-431
Author(s):  
L.S. Cutler
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Submandibular Gland ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Parotid Glands ◽  
Adrenergic Agonist ◽  
Rat Submandibular Gland

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

scholarly journals Developmental Expression of the Peripheral-Type Benzodiazepine Receptor and the Advent of Steroidogenesis in Rat Adrenal Glands*

Endocrinology ◽  
1999 ◽  
Vol 140 (2) ◽  
pp. 859-864 ◽  
Author(s):  
Alexandra Zilz ◽  
Hua Li ◽  
Rosa Castello ◽  
Vassilios Papadopoulos ◽  
Eric P. Widmaier
Keyword(s):  
Ligand Binding ◽  
Binding Capacity ◽  
Benzodiazepine Receptor ◽  
Neonatal Rat ◽  
Developmental Expression ◽  
Neonatal Rats ◽  
Adrenal Cells ◽  
Star Protein ◽  
Peripheral Type

Abstract Although the precise mechanism whereby cholesterol is transported across the outer mitochondrial membrane is uncertain, a multimeric receptor complex termed the peripheral-type benzodiazepine receptor (PBR) appears essential for this process. We therefore predicted that adrenal cells at different developmental stages would express PBR coincidentally with the advent of steroidogenesis. Adrenals of neonatal rats demonstrate greatly reduced sensitivity to ACTH that gradually increases after the first 2 weeks of life. Thus, neonates have lower circulating corticosterone levels following exposure to stress. We examined mitochondrial PBR ligand binding activity, immunoreactive (ir) PBR content, and adrenal sensitivity to ACTH in vivo and in vitro. Ontogeny of both mitochondrial PBR ligand binding capacity and irPBR directly paralleled that of ACTH-inducible steroidogenesis in isolated rat adrenal cells and in rats injected with ACTH. In addition, neonatal PBR had approximately 2-fold higher affinity for PK11195, a synthetic ligand that binds with high affinity to PBR. No correlation was observed during neonatal life between ir-steroidogenic acute regulatory (StAR) protein content and steroidogenesis. These results are consistent with the hypothesis that PBR is an absolute prerequisite for adrenocortical steroidogenesis, and suggest that the stress hyporesponsive period of neonatal rats may result from decreased PBR expression. In addition, the higher affinity of neonatal PBR and the relatively high basal expression of StAR protein in neonatal adrenals may partly explain the high constitutive steroidogenesis characteristic of neonatal rat adrenal cells.

scholarly journals Administration of erythropoietin to newborn rats results in diminished neutrophil production

Blood ◽  
1991 ◽  
Vol 78 (5) ◽  
pp. 1241-1246
Author(s):  
RD Christensen ◽  
KW Liechty ◽  
JM Koenig ◽  
KR Schibler ◽  
RK Ohls
Keyword(s):  
Tritiated Thymidine ◽  
Neonatal Rat ◽  
Newborn Rats ◽  
Suicide Rates ◽  
Colony Forming Units ◽  
High Concentrations ◽  
Macrophage Colony ◽  
High Doses ◽  
Very High

Very high concentrations of erythropoietin (epo), in clonogenic cultures, result in reduced production of neutrophils, and fetal progenitors are more sensitive to this effect of epo than are those of adults. However, the significance of this observation is unclear because no evidence of reduced neutrophil production has been presented following administration of recombinant epo to human or animal subjects. In the present study we injected newborn rats, beginning on the first day of life, with 20, 200, or 2,000 U epo/kg body weight, and measured serum epo concentrations after 2, 8, 24, or 48 hours. After selecting a dose that resulted in serum concentrations greater than 1,000 mU/mL (a concentration that resulted in down-modulation of neutrophil production from neonatal rat progenitors in vitro) other newborn rats were treated for 3 days with that dose (1,000 U epo/kg) or a vehicle control. Administration of epo resulted in increased hematocrits (P less than .001), reticulocyte counts (P less than .001), normoblasts/femur (P less than .05), and normoblasts/spleen (P less than .001). Recipients of epo also had more erythroid colony-forming units (CFU-E) (P less than .001) and higher CFU-E tritiated thymidine suicide rates (P less than .01) than did controls. However, femurs and spleens of epo recipients contained fewer postmitotic neutrophils (femur, P less than .01; spleen, P less than .01), proliferative neutrophils (femur, P less than .01; spleen, P less than .02), granulocyte-macrophage colony-forming units (CFU-GM) (P less than .005), and lower CFU-GM tritiated thymidine suicide rates (P less than .01). Seven and nine days after twice-daily administration of 2,000 U epo/kg, blood neutrophil concentrations had diminished (P less than .05). Thus, administration of high doses of recombinant epo to newborn rats resulted in diminished neutrophil production accompanying accelerated erythropoiesis.

Regulation of Thromboplastin Synthesis in Mouse Placental Cells In Vitro

1983 ◽  
Vol 50 (04) ◽  
pp. 831-834 ◽  
Author(s):  
Knut Dalaker ◽  
Hans Prydz
Keyword(s):  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Low Concentrations ◽  
Placental Cells ◽  
Dose Dependent ◽  
Higher Doses ◽  
Dose Dependent Effect ◽  
Methyl Xanthine

SummaryMouse placental cells are probably constitutive producers of the thromboplastin apoprotein in vitro. The effect of cyclic AMP- elevating compounds on their expression of thromboplastin activity has been studied. Dibutyryl cyclic AMP, the phosphodiesterase inhibitor Ro 20-1724 and the adenyl cyclase stimulator forskolin all decrease the synthesis of thromboplastin. Prostaglandin E2 and the phosphodiesterase inhibitor butyl-methyl-xanthine have a biphasic dose dependent effect. A stimulation was observed at low concentrations, whereas higher doses decreased the synthesis of thromboplastin. Adrenaline had no effect. Combination of two compounds, each at maximally inhibiting concentration gave no significant additive inhibitory effect, showing that they probably act via the same pathway.

Potentiation of NMDA Currents by Pituitary Adenylate Cyclase Activating Polypeptide in Neonatal Rat Sympathetic Preganglionic Neurons

1997 ◽  
Vol 78 (2) ◽  
pp. 1175-1179 ◽  
Author(s):  
S. Y. Wu ◽  
N. J. Dun
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Phosphodiesterase Inhibitor ◽  
Neonatal Rat ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Whole Cell Patch Clamp ◽  
Pituitary Adenylate Cyclase ◽  
Inward Currents ◽  
Induced Currents

Wu, S. Y. and N. J. Dun. Potentiation of NMDA currents by pituitary adenylate cyclase activating polypeptide in neonatal rat sympathetic preganglionic neurons. J. Neurophysiol. 78: 1175–1179, 1997. Whole cell patch-clamp recordings were made from sympathetic preganglionic neurons (SPNs) in the intermediolateral cell column of thoracolumbar spinal cord slices of 12- to 16-day-old rats, and the effects of pituitary adenylate cyclase activating polypeptide (PACAP)-38 on N-methyl-d-aspartate (NMDA)- and kainate (KA)-induced inward currents were examined. PACAP, in concentrations (10–30 nM) that caused no significant change of holding currents, reversibly increased NMDA-induced currents but not KA-induced currents. At higher concentrations (>30 nM), the peptide produced a sustained inward current. The potentiating effect of PACAP was nullified by prior incubation of the slices with the adenylate cyclase inhibitor MDL-12,330A (25 μM). Further, superfusing the slices with the membrane-permeable cyclic AMP analogue N6,2′-0-dibutyryladenosine 3′:5′-cyclic monophosphate (100–300 μM) in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (700 μM) increased the NMDA currents. This result suggests that PACAP selectively increases NMDA-receptor-mediated responses in the rat SPNs, probably via a cyclic-AMP-dependent mechanism, providing evidence that the peptide may be involved in synaptic plasticity.

THE MECHANISM OF ACTION OF PARATHYROID HORMONE: LACK OF EVIDENCE FOR THE MEDIATION BY CYCLIC ADENOSINE 3′, 5′-MONOPHOSPHATE OF PARATHYROID HORMONE-STIMULATED PHOSPHATURIA

1970 ◽  
Vol 46 (2) ◽  
pp. 185-190 ◽  
Author(s):  
J. D. SALLIS
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Mechanism Of Action ◽  
Kidney Tissue ◽  
Adenyl Cyclase ◽  
Cyclase Activity ◽  
Kidney Cortex ◽  
Adenyl Cyclase Activity

SUMMARY The excretion of phosphate in the rat after renal infusion of parathyroid hormone or cyclic adenosine 3,′5′-monophosphate (AMP) is described. The hormone stimulated an immediate phosphaturia, but no such response was measurable in the presence of cyclic AMP. Adenyl cyclase activity in kidney cortex was assessed by measuring the conversion of [14C]adenosine 5′-triphosphate to [14C]cyclic AMP. Previous infusion of kidneys with parathyroid hormone did not alter adenyl cyclase activity but the addition of the hormone to kidney tissue in vitro caused a significant increase in the activity of this enzyme. It is suggested that the parathyroid hormone-stimulated phosphaturia is not mediated by cyclic AMP.

scholarly journals The separate roles of glucose and insulin in the induction of glucokinase in hepatocytes isolated from neonatal rats

1981 ◽  
Vol 196 (2) ◽  
pp. 383-390 ◽  
Author(s):  
M J Wakelam ◽  
D G Walker
Keyword(s):  
Protein Synthesis ◽  
Cyclic Amp ◽  
Actinomycin D ◽  
Neonatal Rats ◽  
Dibutyryl Cyclic Amp ◽  
Subsequent Effect ◽  
Old Rats ◽  
Effect Of Glucose

1. The specificity of the effect of glucose on the induction of glucokinase activity that occurs when hepatocytes freshly isolated from 13-day-old rats are incubated in Medium 199 together with insulin [Wakelam & Walker (1980) FEBS Lett. 111, 115-119] was examined. A pattern that is different from other known effects of glucose is found, and metabolism of this compound is not necessarily to account for this particular effect. 2. The effects of a raised glucose concentration and of insulin on the induction can be separated. The hexose initiates the process in the absence of insulin in a manner that is sensitive to actinomycin D but not to cycloheximide. The subsequent effect of insulin is dependent on the prior effect of glucose or other positive analogue, does not require the presence of glucose and is inhibited by cycloheximide but not by actinomycin D. 3. Induction of glucokinase in vitro in hepatocytes from neonatal animals is inhibited by adrenaline, glucagon and dibutyryl cyclic AMP, but not by vasopressin or angiotensin II. The inhibition by cyclic AMP is on the stage requiring insulin and is comparatively specific, because total protein synthesis is not apparently diminished. 4. The implications of these results are discussed with reference to possible mechanisms of induction and to the situation in vivo.

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