Calcitonin decreases thyrotropin-releasing hormone-stimulated prolactin release through a mechanism that involves inhibition of inositol phosphate production
Autor: | Toshiro Kubota, Jarvis Wd, Bryan L. Spangelo, Allan M. Judd, Son-Iu Kuan, Robert M. MacLeod |
---|---|
Rok vydání: | 1990 |
Předmět: |
Calcitonin
endocrine system medicine.medical_specialty endocrine system diseases Inositol Phosphates Thyrotropin-releasing hormone Arachidonic Acids Biology chemistry.chemical_compound Endocrinology Cytosol Anterior pituitary Pituitary Gland Anterior Internal medicine medicine Cyclic AMP Animals Inositol Calcitonin receptor Inositol phosphate Thyrotropin-Releasing Hormone Cells Cultured Neurotensin chemistry.chemical_classification Forskolin Arachidonic Acid Angiotensin II Colforsin Oxocins Rats Inbred Strains Prolactin Rats medicine.anatomical_structure chemistry Tetradecanoylphorbol Acetate Calcium Female Marine Toxins hormones hormone substitutes and hormone antagonists Vasoactive Intestinal Peptide |
Zdroj: | Endocrinology. 127(1) |
ISSN: | 0013-7227 |
Popis: | Calcitonin is present in both the hypothalamus and pituitary of the rat, and normal rat anterior pituitary cells express calcitonin receptors. Calcitonin has been reported to inhibit or to stimulate PRL release from rat anterior pituitary cells. We have investigated the effects of salmon calcitonin on basal and stimulated PRL release from rat anterior pituitary cells and have studied the effects of this peptide on the intracellular biochemical pathways involved in PRL release. Salmon calcitonin had no significant effect on basal PRL release, but inhibited (P less than 0.01) TRH-stimulated PRL release without affecting PRL release promoted by angiotensin II, neurotensin, phorbol myristate acetate (a protein kinase C activator), or maitotoxin (a calcium channel activator). Salmon calcitonin had no effect on the increase in PRL release and intracellular cAMP concentration after exposure of pituitary cells to vasoactive intestinal peptide or forskolin. Salmon calcitonin significantly decreased (P less than 0.01) the TRH-stimulated rise in inositol phosphates without affecting the angiotensin II-stimulated increase in inositol phosphates. Similarly, salmon calcitonin decreased the TRH-stimulated increase in cytosolic calcium and arachidonate liberation by pituitary cells. We conclude that salmon calcitonin selectively decreases TRH-stimulated PRL release by a mechanism that involves a decrease in inositol phosphate production, as well as a subsequent reduction in cytosolic calcium levels and in arachidonate liberation. |
Databáze: | OpenAIRE |
Externí odkaz: |