Effects of parathyroid hormone, calcitonin, and dibutyryl-cyclic AMP on osteoclast area in cultured chick tibia

2009 ◽  
Vol 5 (7) ◽  
pp. 701-705 ◽  
Author(s):  
Sudha Pandalai ◽  
Carol V. Gay
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Dibutyryl Cyclic Amp ◽  
Chick Tibia

Impaired renal response to parathyroid hormone in potassium depletion

1975 ◽  
Vol 228 (1) ◽  
pp. 179-183 ◽  
Author(s):  
N Beck ◽  
BB Davis
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Potassium Depletion ◽  
Dibutyryl Cyclic Amp ◽  
Renal Response ◽  
Proximal Tubular ◽  
Urinary Cyclic Amp

In potassium depletion, a possible alteration of the proximal tubular response to parathyroid hormone (PTH) was evaluated in rat kidney. 1) There were impairments of both phosphaturic and urinary cyclic AMP responses to PTH. The site of the impairment was further investigated by studying the PTH-dependent cycle AMP system in renal cortex. 2) There was a lesser increase of cyclic AMP concentration by PTH in potassium-depleted slices, indicating the lesser urinary cyclic AMP was due to the specific impairment of PTH-dependent cyclic AMP in the kidney. 3). The activation of adenylate cyclase by PTH was impaired , but phosphodiesterase activity was not affected by potassium depletion, indicating the impairment of cyclic AMP generation was due to inhibition of adenylate cyclase. 4) The phosphaturic response to dibutyryl cyclic AMP infusion was also significantly less in the potassium-depleted animals, indicating the step subsquent to the cyclic AMP generation is also impaired. All above results indicate that, in potassium depletion, the renal response to PTH is impaired, and the impairment is both within the step of cyclic AMP generation and after the cyclic AMP generation.

PTH inhibition of bicarbonate transport by proximal convoluted tubules

1980 ◽  
Vol 239 (2) ◽  
pp. F127-F134 ◽  
Author(s):  
T. D. McKinney ◽  
P. Myers
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Co2 Concentration ◽  
Bicarbonate Transport ◽  
Co2 Absorption ◽  
Fluid Absorption ◽  
Dibutyryl Cyclic Amp ◽  
Convoluted Tubules ◽  
Proximal Convoluted Tubules

These studies examined the effect of parathyroid hormone (PTH), dibutyryl cyclic AMP DBcAMP, and 8-bromo-cyclic AMP BrcAMP on HCO3- transport by rabbit superficial proximal convoluted tubules perfused in vitro. Bicarbonate was estimated as total CO2 measured microcalorimetrically. At slow perfusion rates with 25 mM HCO3- in the perfusate and bath, PTH (0.1 U/ml in the bath) caused the total CO2 in tubular fluid to rise from 10.2 to 19.9 mM. The hormone had no effect on the total CO2 concentration in tubules perfused with HCO3(-)-free perfusates. With HCO3(-) in the perfusate and bath, PTH reduced the rates of fluid and total CO2 absorption to 57 and 48% of control values, respectively. PTH had no effect on the rates of fluid absorption and total CO2 secretion when HCO3(-)-free perfusates were used. The effects of DBcAMP and BrcAMP (10(-7) M in the bath) were similar to those of PTH. 5'-AMP (10(-6) M in the bath) did not alter the total CO2 concentration of tubular fluid when the tubules were perfused at slow rates with HCO3- in the perfusate and bath. Ouabain (10(-5) M in the bath) caused the total CO2 concentration in tubules perfused at slow rates with HCO3--free perfusates to rise from 8.9 to 12.7 mM. PTH caused no further change in the total CO2 concentration in the presence of ouabain.

Interaction between parathyroid hormone and prostaglandin E1 on cyclic AMP metabolism in rat kidney

1980 ◽  
Vol 93 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Naokazu Nagata ◽  
Yuriko Ono ◽  
Narimichi Kimura
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Rat Kidney ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Newborn Rat ◽  
Simultaneous Addition ◽  
Renal Cortical Tissue ◽  
Subsequent Addition

Abstract. The interaction between parathyroid hormone (PTH) and prostaglandin E1 (PGE1) in influencing cyclic AMP metabolism in rat renal cortical tissue was examined. PTH and PGE1 stimulated additively the adenylate cyclase activity in the homogenate of the tissue. Both PTH and PGE1 enhanced the level of cyclic AMP in the incubated renal cortical tissue, but the effect of their simultaneous addition did not exceed the effect induced by PTH alone. Cyclic AMP accumulated in the incubation medium by stimulation by PTH was decreased by the simultaneous addition of PGE1. When the tissue was pre-incubated for 30 min with 2 to 10 μg/ml of PGE1, the magnitude of the increase of cyclic AMP caused by PTH subsequently added was lessened. However, the response to PTH of adenylate cyclase preparation obtained from the homogenate of PGE1-pre-treated tissue was not decreased. When first PTH was added to the incubating renal cortical tissue, the subsequent addition of PGE1 accelerated the decrease of cyclic AMP content in the tissue and decreased the amount of cyclic AMP released from the tissue. The interaction of PTH and PGE1 on cyclic AMP metabolism in the renal cortical tissue was in contrast to that seen in newborn rat calvaria where PGE1 and PTH acted additively in enhancing the level of cyclic AMP.

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