Human placental lactogen release in vitro: paradoxical effects of calcium

1981 ◽  
Vol 240 (5) ◽  
pp. E550-E555
Author(s):  
S. Handwerger ◽  
P. M. Conn ◽  
J. Barrett ◽  
S. Barry ◽  
A. Golander
Keyword(s):  
Calcium Influx ◽  
Extracellular Calcium ◽  
Calcium Flux ◽  
Placental Lactogen ◽  
Human Placental Lactogen ◽  
Paradoxical Effects ◽  
Subsequent Exposure ◽  
Normal Calcium

To study the effects of calcium on the release of human placental lactogen (hPL), placental explants were exposed to media containing lower or higher concentrations of calcium than normally available to the placenta. Explants exposed for 2 h to calcium-poor medium or medium containing either 2 mM EDTA or 2 mM EGTA released 160, 248, and 253% more hPL, respectively, than control explants. In contrast, explants exposed to medium containing higher than normal calcium concentrations released the same amounts of hPL as the control explants. At lower than normal extracellular calcium concentrations, the increased hPL release was inversely proportional to the calcium concentration. The increased release in calcium-poor medium was inhibited by subsequent exposure of the explants to medium containing calcium and was prevented by either barium or magnesium. Changes in barium or magnesium concentrations, however, had no effects on hPL release in the presence of normal extracellular calcium concentrations. Methoxyverapamil (D 600), an inhibitor of calcium flux, stimulated hPL release. Because low extracellular calcium and methoxyverapamil both inhibit calcium influx, these experiments suggest that calcium influx inhibits hPL release. The role of calcium in the regulation of hPL release therefore appears to be different from that reported in other release systems.

Failure of Human Growth Hormone and Human Placental Lactogen to Affect Glucose Consumption by Human Erythrocytes and Leucocytes In Vitro

1972 ◽  
Vol 50 (10) ◽  
pp. 1014-1017
Author(s):  
Catherine L. Tanser ◽  
Nannie K. M. de Leeuw
Keyword(s):  
Growth Hormone ◽  
Glucose Oxidase ◽  
Human Growth Hormone ◽  
Glucose Utilization ◽  
Human Growth ◽  
Glucose Consumption ◽  
Inhibitory Effect ◽  
Placental Lactogen ◽  
Human Placental Lactogen

The effect of human growth hormone (HGH) and human placental lactogen (HPL) on glucose consumption by erythrocytes and leucocytes in vitro was investigated. Glucose consumption was measured by determining glucose utilization during 3 h incubation at 37 °C, using the glucose oxidase method.HGH and HPL showed no effect on glucose consumption by erythrocytes, and HPL showed no effect on glucose consumption by leucocytes in vitro. Our results do not confirm previous reports of an inhibitory effect of HGH on glucose consumption by erythrocytes in vitro.

Acidosis inhibits osteoblastic and stimulates osteoclastic activity in vitro

1992 ◽  
Vol 262 (3) ◽  
pp. F442-F448 ◽  
Author(s):  
N. S. Krieger ◽  
N. E. Sessler ◽  
D. A. Bushinsky
Keyword(s):  
Alkaline Phosphatase ◽  
Metabolic Acidosis ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Collagen Synthesis ◽  
Calcium Flux ◽  
Osteoclastic Activity ◽  
Glucuronidase Activity

Metabolic acidosis induces net calcium flux (JCa) from cultured neonatal mouse calvariae through physicochemical and cell-mediated mechanisms. To determine the role of osteoblasts in acid-induced JCa, collagen synthesis and alkaline phosphatase activity were assessed in calvariae incubated in reduced pH and bicarbonate medium, a model of metabolic acidosis (Met), and compared with controls (Ctl). Collagen synthesis fell from 30.5 +/- 1.1 in Ctl to 25.1 +/- 0.4% with Met, and alkaline phosphatase decreased from 403 +/- 25 in Ctl to 298 +/- 21 nmol Pi.min-1.mg protein-1 with Met. During acidosis JCa was correlated inversely with percent collagen synthesis (r = -0.743, n = 11, P = 0.009) and with alkaline phosphatase activity (r = -0.453, n = 22, P = 0.034). To determine the role of osteoclasts in acid-induced JCa, osteoclastic beta-glucuronidase activity was determined in Ctl and Met in the absence or presence of the osteoclastic inhibitor calcitonin (CT, 3 x 10(-9) M). Met increased beta-glucuronidase (5.9 +/- 0.2) compared with Ctl (4.6 +/- 0.3 micrograms phenolphthalein released.bone-1.h-1), whereas CT inhibited beta-glucuronidase in both Ctl and Met (3.1 +/- 0.2 and 3.5 +/- 0.3, respectively). During acidosis JCa was correlated directly with beta-glucuronidase activity (r = 0.683, n = 42, P less than 0.001). Thus the cell-mediated component of JCa during acidosis in vitro appears to result from a combination of inhibited osteoblastic and stimulated osteoclastic activity.

Role of sodium ion gradient in facilitating extracellular calcium influx

1991 ◽  
Vol 64 (2) ◽  
pp. 179-190 ◽  
Author(s):  
Yukio Ozaki ◽  
Yuki Jinnai ◽  
Yutaka Yatomi ◽  
Shoji Kume
Keyword(s):  
Calcium Influx ◽  
Extracellular Calcium ◽  
Sodium Ion ◽  
Ion Gradient

EFFECT OF IONIC ENVIRONMENT ON THE RELEASE OF HUMAN PLACENTAL LACTOGEN IN VITRO

1976 ◽  
Vol 69 (3) ◽  
pp. 349-358 ◽  
Author(s):  
V. J. CHOY ◽  
W. B. WATKINS
Keyword(s):  
Placental Tissue ◽  
Placental Lactogen ◽  
Human Placental Lactogen ◽  
Short Term ◽  
Graded Response ◽  
High K ◽  
Human Placental Tissue ◽  
High Concentrations ◽  
Free Media

SUMMARY Short-term incubation of human placental tissue in Krebs–Ringer bicarbonate buffered media with various concentrations of K+ and Ca2+ showed a graded response in human placental lactogen (HPL) release at different Ca2+ concentrations, but no effect at increased K+ concentration. Media with high Ca2+ caused an inhibition of release, while Ca2+-free media caused a stimulation in HPL release. High concentrations of Mg2+ inhibited release minimally, while Ba2+ had no effect. There was no change in HPL release when Na+ concentration was increased. La3+-Locke's solution markedly inhibited release of HPL but the significance of this effect is unknown. These results suggest that Ca2+ is not required for HPL secretion from placental tissue. It seems that HPL secretion in vitro does not follow the usual pattern where a physiological stimulus or high K+ concentration causes inward movement of calcium which couples stimulation to secretion.

Role of extracellular calcium influx in EGF-induced osteoblastic cell proliferation

Bone ◽  
1995 ◽  
Vol 16 (4) ◽  
pp. S341-S347 ◽  
Author(s):  
J. Loza ◽  
L. Carpio ◽  
G. Lawless ◽  
N. Marzec ◽  
R. Dziak
Keyword(s):  
Cell Proliferation ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Osteoblastic Cell

Urinary Oestrogen and Plasma Human Placental Lactogen as Initial Screening Tests for a Placental Sulphatase Deficiency

1976 ◽  
Vol 21 (3) ◽  
pp. 106-108 ◽  
Author(s):  
G. H. Beastall ◽  
Anne M. Kelly ◽  
P. England ◽  
L. G. S. Rao ◽  
Margaret W. Macgregor ◽  
...  
Keyword(s):  
Enzyme Activities ◽  
Routine Screening ◽  
In Vitro Studies ◽  
Placental Lactogen ◽  
Screening Tests ◽  
Human Placental Lactogen ◽  
Initial Screening

As a result of routine screening of ante-natal patients by urinary total oestrogens and plasma human placental lactogen (HPL) from 35 weeks, a rare placental sulphatase deficiency was indicated which was later confirmed by in vitro studies of placental enzyme activities.

The contractile action of platelet-activating factor on gallbladder smooth muscle

2000 ◽  
Vol 279 (1) ◽  
pp. G67-G72 ◽  
Author(s):  
Henry P. Parkman ◽  
Arlene N. James ◽  
James P. Ryan
Keyword(s):  
Pertussis Toxin ◽  
Contractile Response ◽  
Calcium Influx ◽  
Platelet Activating Factor ◽  
Extracellular Calcium ◽  
Motor Dysfunction ◽  
Gallbladder Contraction ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Platelet-activating factor (PAF) may be a mediator of some sequelae of cholecystitis, a disorder with gallbladder motor dysfunction. The aims of this study were to determine the effect and mechanism of PAF on gallbladder muscle. Exogenous administration of PAF-16 or PAF-18 caused dose-dependent contractions of gallbladder muscle strips in vitro with threshold doses of 1 ng/ml and 10 ng/ml, respectively. The PAF-induced contractions were not significantly reduced by TTX, atropine, or hexamethonium but were significantly inhibited with the PAF receptor antagonists ginkolide B and CV-3988. The PAF-induced contraction was reduced by indomethacin. Preventing influx of extracellular calcium with a calcium-free solution nearly abolished the PAF contractile response. Nifedipine inhibited the PAF contractile response, whereas ryanodine had no effect. Pertussis toxin reduced the PAF contractile response. In conclusion, PAF causes gallbladder contraction through specific PAF receptors on gallbladder muscle. These PAF receptors appear to be linked to a prostaglandin-mediated mechanism and to pertussis toxin-sensitive G proteins. The contractile response is largely mediated through the utilization of extracellular calcium influx through voltage-dependent calcium channels.

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