Vitamin D-enhanced thyrotrophin release from rat pituitary cells: effects of Ca2+, dihydropyridines and ionomycin

Abstract

Vitamin D may regulate pituitary function, as there are selective effects of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on gene expression in clonal pituitary tumour cells, and on TRH-induced TSH release in normal rat pituitary cells in vitro. The role of Ca2+ in 1,25-(OH)2D3-enhanced TSH release from primary rat pituitary cell cultures was investigated. Pretreatment with 10 nmol 1,25-(OH)2D3/l for 24 h augmented KCl (3-60 mmol/l)-induced TSH release over 1 h at all KCl concentrations greater than 7.5 mmol/l (P less than 0.001), with a 76% enhancement of TSH release induced by 30 mmol KCl/l (P less than 0.001). The Ca2+ channel antagonist nifedipine (10 nmol/l-10 mumol/l) caused a concentration-dependent inhibition of KCl (60 mmol/l)-induced TSH secretion. Pretreatment with 1,25-(OH)2D3 enhanced KCl-induced release at all concentrations of nifedipine (P less than 0.001). The Ca2+ selective divalent cation ionophore ionomycin (1 nmol/l-1 mumol/l), and the Ca2+ channel agonist BAY K 8644 (10 nmol/l-1 mumol/l) increased prolactin secretion but did not increase TSH release, and 1,25-(OH)2D3 had no effect. At an extracellular Ca2+ concentration of less than 500 nmol/l, TRH-induced TSH release was observed only after treatment with 1,25-(OH)2D3 (P less than 0.01). As the extracellular Ca2+ concentration was increased, greater increments of TRH-induced TSH release were observed following pretreatment with 1,25-(OH)2D3 (P less than 0.01). However, the effect of 1,25-(OH)2D3 in the thyrotroph was independent of the pretreatment extracellular Ca2+ concentration. We have shown that 1,25-(OH)2D3 acts selectively on the thyrotroph to enhance in-vitro responsiveness to TRH and KCl. These data suggest that the action of 1,25-(OH)2D3 in the thyrotroph is to enhance intracellular signal transduction. They further support a permissive or regulatory role of vitamin D in the normal pituitary gland.

Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency

“…The VDR messenger RNA (mRNA) expression has been demonstrated in the human pituitary gland, suggesting the possibility that, like in the rat pituitary, VDR may regulate the human pituitary gene expression and hormone secretion [14,15].…”

Genomic mechanisms involved in the pleiotropic actions of 1,25-dihydroxyvitamin D3

“…A functional VDRE was identified in the human p21 promoter (AGGGAGattGGTTCA ; k779 to k765). reported to enhance the agonist-induced secretion of both prolactin and thyroid-stimulating hormone [160,161]. In addition to affecting hormone secretion from the parathyroid and pituitary glands, 1,25(OH) # D $ has also been reported to enhance pancreatic insulin secretion [162][163][164].…”

Relationship between gestational transient thyrotoxicosis and vitamin D

“…Sar et al suggested a central effect of vit D on the modulation of thyrotropin secretion in the pituitary gland (13). Administration of vit D has been reported to increase thyrotropin-releasing hormone-induced TSH secretion in rats (17). In another study, vit D level was increased after administration of T3, T4, and TSH in rats (18).…”