Parathyroid hormone inhibition of induction of alkaline phosphatase activity in HeLa cells by 5-iodo-2′-deoxyuridine without increased adenylate cyclase activity or cellular cAMP concentration

1980 ◽  
Vol 129 (2) ◽  
pp. 425-430 ◽  
Author(s):  
Cathryn A. Hart ◽  
Walker Wharton ◽  
Barry Goz
Keyword(s):  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Adenylate Cyclase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Hela Cells ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Camp Concentration

Selective inhibition by epinephrine of parathyroid hormone-stimulated adenylate cyclase in rat renal cortex

1982 ◽  
Vol 242 (6) ◽  
pp. F721-F726 ◽  
Author(s):  
E. A. Woodcock ◽  
C. I. Johnston
Keyword(s):  
Parathyroid Hormone ◽  
Adenylate Cyclase ◽  
Renal Cortex ◽  
Selective Inhibition ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Renal Tubules ◽  
Direct Inhibition ◽  
Basal Activity ◽  
Absolute Decrease

Parathyroid hormone- (PTH) stimulated adenylate cyclase activity in homogenates of rat renal cortex was inhibited by l-epinephrine. The specificity of the inhibition indicated that it was mediated by alpha 2-receptors. The inhibition of PTH-stimulated activity was greater than the inhibition of basal activity. The absolute decrease in adenylate cyclase activity produced by 10-4 M l-epinephrine was from 16.3 +/-0.6 (SE) to 11.2 +/- 0.6 pmol.min-1.mg-1 for activity stimulated by 10 microgram/ml PTH. Basal activity was decreased from 2.3 +/- 0.07 to 1.7 +/- 0.04. A similar inhibition of PTH-stimulated adenylate cyclase by l-epinephrine was demonstrated in preparations of renal cortical tubules. In contrast, the quantitative decrease in vasopressin-or calcitonin-stimulated activity by 10-4 M l-epinephrine was the same as the decrease in basal activity. These results demonstrate that PTH receptors that stimulated adenylate cyclase and alpha 2-adrenergic receptors that inhibit adenylate cyclase are present on the same cells in the renal tubules. Thus, a mechanism exists whereby alpha-adrenergic agonists can oppose the tubular actions of PTH via a direct inhibition of adenylate cyclase activity.

Induction of alkaline phosphatase activity in HeLa cells by sodium butyrate

In Vitro ◽  
1979 ◽  
Vol 15 (11) ◽  
pp. 861-864 ◽  
Author(s):  
Walker Wharton ◽  
Cathryn A. Hart ◽  
Barry Goz
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Sodium Butyrate ◽  
Hela Cells

Low-dose parathyroid hormone and estrogen reverse alkaline phosphatase activity suppressed by dexamethasone in mouse osteoblastic cells

2005 ◽  
Vol 23 (6) ◽  
pp. 450-455 ◽  
Author(s):  
Mei-Fway Iu ◽  
Hiroshi Kaji ◽  
Junko Naito ◽  
Hideaki Sowa ◽  
Toshitsugu Sugimoto ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Low Dose ◽  
Osteoblastic Cells

scholarly journals ALKALINE PHOSPHATASE ACTIVITY IN HELA CELLS

1967 ◽  
Vol 15 (7) ◽  
pp. 417-418 ◽  
Author(s):  
J. HUGON ◽  
M. BORGERS ◽  
M. C. LONI
Keyword(s):  
Alkaline Phosphatase ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Hela Cells

EVIDENCE FOR A SEPARATE ADENYLATE CYCLASE SYSTEM RESPONSIVE TO BETA-ADRENERGIC STIMULATION IN THE RENAL CORTEX OF THE RAT

1974 ◽  
Vol 77 (3) ◽  
pp. 604-611 ◽  
Author(s):  
Norman H. Bell ◽  
John Fleming ◽  
Joanne Benedict ◽  
Lisa Pantzer
Keyword(s):  
Parathyroid Hormone ◽  
Adenylate Cyclase ◽  
Renal Cortex ◽  
Blocking Agent ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Adenylate Cyclase System ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Increased Activity

ABSTRACT Previous studies in other laboratories had indicated that some of the effects of parathyroid hormone on skeletal tissue and the renal tubule to influence ion metabolism can be produced by beta-adrenergic stimulation. Studies were carried out to determine whether the same adenylate cyclase system in rat renal cortex is activated by parathyroid hormone and isoproterenol. At maximal effective concentration of dose response, parathyroid hormone (2 × −5 m) increased adenylate cyclase activity by some 415 per cent, isoproterenol (10−6 m) increased activity by some 40 to 50 per cent, vasopressin (10−5 m) increased activity by some 96 per cent and porcine calcitonin (10−5 m) increased activity by some 92 per cent. Dl-propranolol (10−5 m), a beta-adrenergic receptor blocking agent, prevented the increase in enzyme activity produced by isoproterenol (10−6 m), did not diminish the increase in activity produced by parathyroid hormone (10−6 m) and did not influence basal adenylate cyclase activity by itself. The combined maximal concentrations of isoproterenol together with either parathyroid hormone, vasopressin or porcine calcitonin were additive. These results indicate that there is an adenylate cyclase system in rat renal cortex which can be activated by beta-adrenergic stimulation with isoproterenol, and is separate from the systems responsive to parathyroid hormone, vasopressin or calcitonin.

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