Growth hormone-releasing factor-44 specificity for components of somatotroph and lactotroph immediate release pool substructures

M. E. Stachura, J. M. Tyler

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Rat somatotroph and lactotroph hormone storage is divisible into at least two functional compartments: an immediate release pool (IRP) and a pool that responds to prolonged stimulation. An IRP substructure has been defined by release in response to potassium ion (K+), prostaglandin Ei (PGE1), and Bu2cAMP. The somatotroph IRP is expandable; the lactotroph IRP is fixed in size. The present experiments examined which IRP components contribute to the rapid release of stored GH in response to GH-releasing factor-44 (GRF). Release of stored PRL was monitored for comparison. In vitro prelabeling defined stored rat (r) GH and rPRL. Release in response to 21 DIM K+, 3 μM PGE1(1 mM Bu2cAMP, and/or 3 nM GRF was monitored with a perifusion-immunoprecipitation system. After 120 min of basal perifusion, tissue was exposed to one of the four secretagogues for 90 min. During a second 90-min period a second secretagogue was added while exposure to the first secretagogue continued. We demonstrated that 1) 21 mM K+ reduces peak rGH release in response to 3 nM GRF by 52%, whereas GRF does not reduce rGH release in response to K+; 2) 3 μM PGE1 reduces rGH release in response to GRF by only 19% although GRF reduces rGH release in response to PGEi by 88%; 3) 1 mM Bu2cAMP reduces rGH release in response to GRF by 87%, and GRF eliminates rGH release in response to Bu2cAMP (1.2% of control value); 4) combined K+ plus Bu2cAMP reduce rGH release in response to GRF to 2.5% of the control value, whereas after GRF pretreatment rGH release in response to combined K+ plus Bu2cAMP is 93% of the control value; and 5) combined PGEi and Bu2cAMP reduce the response to GRF to 17% of the control value. Effects on rPRL release are qualitatively similar. We conclude that immediate GRF-stimulated release of stored rGH originates in the somatotroph IRP components defined by responses to PGE1 and Bu2cAMP; it derives only slightly, if at all, from the IRP component defined by the response to K+. The smaller GRF-stimulated release of IRP rPRL is similarly derived.

Original languageEnglish (US)
Pages (from-to)1719-1726
Number of pages8
JournalEndocrinology
Volume120
Issue number5
DOIs
StatePublished - Jan 1 1987

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Lactotrophs
Somatotrophs
Growth Hormone-Releasing Hormone
Alprostadil
Immunoprecipitation
Prostaglandins
Potassium
Hormones
Ions

ASJC Scopus subject areas

  • Endocrinology

Cite this

Growth hormone-releasing factor-44 specificity for components of somatotroph and lactotroph immediate release pool substructures. / Stachura, M. E.; Tyler, J. M.

In: Endocrinology, Vol. 120, No. 5, 01.01.1987, p. 1719-1726.

Research output: Contribution to journalArticle

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abstract = "Rat somatotroph and lactotroph hormone storage is divisible into at least two functional compartments: an immediate release pool (IRP) and a pool that responds to prolonged stimulation. An IRP substructure has been defined by release in response to potassium ion (K+), prostaglandin Ei (PGE1), and Bu2cAMP. The somatotroph IRP is expandable; the lactotroph IRP is fixed in size. The present experiments examined which IRP components contribute to the rapid release of stored GH in response to GH-releasing factor-44 (GRF). Release of stored PRL was monitored for comparison. In vitro prelabeling defined stored rat (r) GH and rPRL. Release in response to 21 DIM K+, 3 {\^I}¼M PGE1(1 mM Bu2cAMP, and/or 3 nM GRF was monitored with a perifusion-immunoprecipitation system. After 120 min of basal perifusion, tissue was exposed to one of the four secretagogues for 90 min. During a second 90-min period a second secretagogue was added while exposure to the first secretagogue continued. We demonstrated that 1) 21 mM K+ reduces peak rGH release in response to 3 nM GRF by 52{\%}, whereas GRF does not reduce rGH release in response to K+; 2) 3 {\^I}¼M PGE1 reduces rGH release in response to GRF by only 19{\%} although GRF reduces rGH release in response to PGEi by 88{\%}; 3) 1 mM Bu2cAMP reduces rGH release in response to GRF by 87{\%}, and GRF eliminates rGH release in response to Bu2cAMP (1.2{\%} of control value); 4) combined K+ plus Bu2cAMP reduce rGH release in response to GRF to 2.5{\%} of the control value, whereas after GRF pretreatment rGH release in response to combined K+ plus Bu2cAMP is 93{\%} of the control value; and 5) combined PGEi and Bu2cAMP reduce the response to GRF to 17{\%} of the control value. Effects on rPRL release are qualitatively similar. We conclude that immediate GRF-stimulated release of stored rGH originates in the somatotroph IRP components defined by responses to PGE1 and Bu2cAMP; it derives only slightly, if at all, from the IRP component defined by the response to K+. The smaller GRF-stimulated release of IRP rPRL is similarly derived.",
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N2 - Rat somatotroph and lactotroph hormone storage is divisible into at least two functional compartments: an immediate release pool (IRP) and a pool that responds to prolonged stimulation. An IRP substructure has been defined by release in response to potassium ion (K+), prostaglandin Ei (PGE1), and Bu2cAMP. The somatotroph IRP is expandable; the lactotroph IRP is fixed in size. The present experiments examined which IRP components contribute to the rapid release of stored GH in response to GH-releasing factor-44 (GRF). Release of stored PRL was monitored for comparison. In vitro prelabeling defined stored rat (r) GH and rPRL. Release in response to 21 DIM K+, 3 μM PGE1(1 mM Bu2cAMP, and/or 3 nM GRF was monitored with a perifusion-immunoprecipitation system. After 120 min of basal perifusion, tissue was exposed to one of the four secretagogues for 90 min. During a second 90-min period a second secretagogue was added while exposure to the first secretagogue continued. We demonstrated that 1) 21 mM K+ reduces peak rGH release in response to 3 nM GRF by 52%, whereas GRF does not reduce rGH release in response to K+; 2) 3 μM PGE1 reduces rGH release in response to GRF by only 19% although GRF reduces rGH release in response to PGEi by 88%; 3) 1 mM Bu2cAMP reduces rGH release in response to GRF by 87%, and GRF eliminates rGH release in response to Bu2cAMP (1.2% of control value); 4) combined K+ plus Bu2cAMP reduce rGH release in response to GRF to 2.5% of the control value, whereas after GRF pretreatment rGH release in response to combined K+ plus Bu2cAMP is 93% of the control value; and 5) combined PGEi and Bu2cAMP reduce the response to GRF to 17% of the control value. Effects on rPRL release are qualitatively similar. We conclude that immediate GRF-stimulated release of stored rGH originates in the somatotroph IRP components defined by responses to PGE1 and Bu2cAMP; it derives only slightly, if at all, from the IRP component defined by the response to K+. The smaller GRF-stimulated release of IRP rPRL is similarly derived.

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