Ionophore A23187 promotes osteoclast formation in bone organ culture

1982 ◽  
Vol 34 (1) ◽  
pp. 31-36 ◽  
Author(s):  
P. H. Stern ◽  
M. F. Orr ◽  
E. Brull
Keyword(s):  
Organ Culture ◽  
Osteoclast Formation ◽  
Ionophore A23187 ◽  
Bone Organ Culture

Studies of lead transport in bone organ culture

1977 ◽  
Vol 26 (7) ◽  
pp. 650-652 ◽  
Author(s):  
John F. Rosen ◽  
Emma E. Wexler
Keyword(s):  
Organ Culture ◽  
Bone Organ Culture

Ametantrone inhibits prostaglandin — mediated resorption in bone organ culture

1984 ◽  
Vol 28 (4) ◽  
pp. 469-476 ◽  
Author(s):  
Margaret R. Warner ◽  
Mark S. Rappaport ◽  
Nancy S. Krieger ◽  
Raymond F. Novak ◽  
Paula H. Stern
Keyword(s):  
Organ Culture ◽  
Bone Organ Culture

Calcium-independent stimulation of glycogenolysis by arginine vasotocin and catecholamines in liver of the axolotl (Ambystoma mexicanum) in vitro

1986 ◽  
Vol 109 (1) ◽  
pp. 75-84 ◽  
Author(s):  
P. A. Janssens ◽  
J. Kleineke ◽  
A. G. Caine
Keyword(s):  
Organ Culture ◽  
Calcium Ionophore ◽  
Phosphodiesterase Inhibitors ◽  
Calcium Ionophore A23187 ◽  
Ambystoma Mexicanum ◽  
Arginine Vasotocin ◽  
Maximal Response ◽  
Ionophore A23187 ◽  
Glucose Release

ABSTRACT Arginine vasotocin (AVT) caused a concentrationdependent increase of glycogen phosphorylase a activity, breakdown of glycogen and release of glucose, when added to pieces of axolotl liver in organ culture. The concentration causing half-maximal response (EC50) was about 1 nmol/l. These actions of AVT were unaffected by the adrenergic antagonists propranolol, yohimbine and prazosin, but were blocked by equimolar amounts of d(CH2)5Tyr(Me)AVT, a synthetic antagonist of vasopressin. Arginine vasotocin similarly caused glycogenolysis in isolated perfused axolotl liver where the EC50 was about 0·1 nmol/l. The glycogenolytic action of AVT (10 nmol/l) was sustained for at least 3 h in Ca2+ -free perfusion and longer in organ culture. No increase in Ca2+ concentration in the effluent perfusion medium was apparent during AVT-induced glucose release. Omission of Ca2+ from the medium, together with addition of EGTA (2·5 mmol/l) to the organ culture, had only a slight inhibitory effect upon the rate of glycogenolysis brought about by AVT and did not inhibit the glycogenolytic action of catecholamines. Addition of the calcium ionophore A23187 (5 μmol/l) neither caused glucose release nor abolished the glycogenolytic action of AVT added subsequently. Nevertheless, A23187 caused increased loss of 45Ca from Ca2+-loaded liver pieces whereas AVT was without effect. There was a slight accumulation of cyclic AMP (cAMP), but not cGMP, in axolotl liver pieces cultured in the presence of 0·1 μmol AVT/l and this was accentuated in the presence of phosphodiesterase inhibitors. We conclude that, in contrast to the position in mammals, Ca2+ is not involved in the glycogenolytic actions of AVT or catecholamines in axolotl liver. Preliminary experiments suggest that the same is true in the carp and we suggest that the involvement of Ca2+ in regulation of hepatic glucose release may not have evolved until after the amphibians separated from the ancestors of the mammals. J. Endocr. (1986) 109, 75–84

scholarly journals Cardiotonic agent milrinone stimulates resorption in rodent bone organ culture.

1987 ◽  
Vol 79 (2) ◽  
pp. 444-448 ◽  
Author(s):  
N S Krieger ◽  
T S Stappenbeck ◽  
P H Stern
Keyword(s):  
Organ Culture ◽  
Cardiotonic Agent ◽  
Bone Organ Culture

Role of calcium in osmotic and nonosmotic release of vasopressin from rat organ culture

1983 ◽  
Vol 244 (5) ◽  
pp. R703-R708
Author(s):  
S. Ishikawa ◽  
R. W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Organ Culture ◽  
Arginine Vasopressin ◽  
Ionophore A23187 ◽  
Ang Ii ◽  
Ca Uptake ◽  
High Concentrations ◽  
Cellular Ca ◽  
Stimulation Of

In the present study the role of calcium (Ca) in the stimulation of arginine vasopressin (AVP) release from the cultured rat hypothalamoneurohypophyseal complex (HNC) was examined in response to three different stimuli, 56 mM potassium chloride, an increase in medium osmolality from 290 to 310 mosmol/kg H2O, or 1 X 10(-6) M angiotensin II (ANG II). With all three stimuli AVP release from rat HNC explants was enhanced by increasing Ca concentration in the medium from 0 to 1.8 mM Ca. However, high concentrations of Ca (8 mM) inhibited the response of AVP release to either hyperosmolality or angiotensin II. Chemically dissimilar blockers of cellular Ca uptake, verapamil (5.2 X 10(-6) or 5.2 X 10(-5) M) or nifedipine (5.8 X 10(-6) or 5.8 X 10(-5) M), completely abolished AVP release from rat HNC explants in response to the three different stimuli in 1.8 mM Ca. In a normal concentration of medium Ca (1.8 mM) a Ca ionophore, A23187 (3.8 X 10(-5) M), significantly enhanced the osmotic and nonosmotic (ANG II-stimulated) release of AVP from rat HNC explants compared with controls without Ca ionophore. This effect of Ca ionophore to enhance AVP release was more evident in a lower Ca medium (0.9 mM Ca in the hyperosmolality study and 0.3 mM Ca in the ANG II study). These results therefore indicate that cellular Ca uptake is an important modulator of osmotic and nonosmotic AVP release from the intact rat hypothalamoneurohypophyseal system. The influence of extracellular Ca on the osmotic and nonosmotic release of AVP is also demonstrated.

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