Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187

Thomas Yorio; Sheryl L. Henry; Donald H. Hodges; James L. Caffrey

doi:10.1016/0006-2952(83)90634-2

Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187

Thomas Yorio, Sheryl L. Henry, Donald H. Hodges, James L. Caffrey

Research output: Contribution to journal › Article › peer-review

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Abstract

The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E₂ (PGE₂). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.

Original language	English
Pages (from-to)	1113-1118
Number of pages	6
Journal	Biochemical Pharmacology
Volume	32
Issue number	6
DOIs	https://doi.org/10.1016/0006-2952(83)90634-2
State	Published - 15 Mar 1983

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title = "Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187",

abstract = "The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E2 (PGE2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.",

author = "Thomas Yorio and Henry, {Sheryl L.} and Hodges, {Donald H.} and Caffrey, {James L.}",

note = "Funding Information: Cyclic AMP, as well as phosphodiesterase inhibitors, mimics the action of antidiuretic hormone when added exogenously. The hydro-osmotic response to exogenous cyclic AMP was unaffected by ionophore, while that due to 3-isobutyl-l-methylxanthine and dibutyryl cyclic AMP was considerably reduced. The effect of dibutyryl cAMP is probably not solely exerted by mimicking endogenous nucleotide but also through inhibition of phosphodiesterase. Such a dual action would help explain the large discrepancy between the abilities of the IP to block the db-cAMP and not the exogenous cyclic AMP response. This concept is supported by the action of the ionophore to inhibit the methylxanthine-mediated hydro-osmotic response. This clear inhibition of the db-cAMP hydro-osmotic response suggests that the indirect effect of db-cAMP on the accumulation of endogenous cyclic AMP may be its predominant action.",

year = "1983",

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T1 - Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187

AU - Yorio, Thomas

AU - Henry, Sheryl L.

AU - Hodges, Donald H.

AU - Caffrey, James L.

N1 - Funding Information: Cyclic AMP, as well as phosphodiesterase inhibitors, mimics the action of antidiuretic hormone when added exogenously. The hydro-osmotic response to exogenous cyclic AMP was unaffected by ionophore, while that due to 3-isobutyl-l-methylxanthine and dibutyryl cyclic AMP was considerably reduced. The effect of dibutyryl cAMP is probably not solely exerted by mimicking endogenous nucleotide but also through inhibition of phosphodiesterase. Such a dual action would help explain the large discrepancy between the abilities of the IP to block the db-cAMP and not the exogenous cyclic AMP response. This concept is supported by the action of the ionophore to inhibit the methylxanthine-mediated hydro-osmotic response. This clear inhibition of the db-cAMP hydro-osmotic response suggests that the indirect effect of db-cAMP on the accumulation of endogenous cyclic AMP may be its predominant action.

PY - 1983/3/15

Y1 - 1983/3/15

N2 - The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E2 (PGE2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.

AB - The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E2 (PGE2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.

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JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

IS - 6

ER -

Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187

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