Effects of gastrin-releasing peptide on basal and stimulated thyroid hormone secretion in the mouse
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1Department of Pharmacology, Lund University, Sweden.
Recently, gastrin releasing peptide (GRP) was demonstrated to occur within normal thyroidal C cells. In the present study, the effects of GRP on basal and stimulated thyroid hormone secretion were investigated in the mouse according to the McKenzie technique. Iodine-deficient mice were pretreated with 125I and thyroxine. GRP was found dose-dependently to increase the basal radioiodine levels after iv injection, reflecting a stimulation of basal thyroid hormone secretion. The effect was maximal at a dose level of 3.0 nmol/animal, and at 2 h after injection, when GRP had increased blood radioiodine levels to 152 +/- 8% compared with 96 +/- 5% in controls (P less than 0.001). GRP seemed to exert additive effects on thyroid hormone secretion with vasoactive intestinal peptide and with TSH at a threshold dose level. In contrast, GRP did not influence the stimulatory effects of either a half-maximal dose level of TSH or noradrenaline. Furthermore, neither L-propranolol nor methylatropine influenced the GRP-induced thyroid hormone secretion. It is concluded that GRP has the capacity to stimulate basal thyroid hormone secretion in the mouse.
Recently, gastrin releasing peptide (GRP) was demonstrated to occur within normal thyroidal C cells. In the present study, the effects of GRP on basal and stimulated thyroid hormone secretion were investigated in the mouse according to the McKenzie technique. Iodine-deficient mice were pretreated with 125I and thyroxine. GRP was found dose-dependently to increase the basal radioiodine levels after iv injection, reflecting a stimulation of basal thyroid hormone secretion. The effect was maximal at a dose level of 3.0 nmol/animal, and at 2 h after injection, when GRP had increased blood radioiodine levels to 152 +/- 8% compared with 96 +/- 5% in controls (P less than 0.001). GRP seemed to exert additive effects on thyroid hormone secretion with vasoactive intestinal peptide and with TSH at a threshold dose level. In contrast, GRP did not influence the stimulatory effects of either a half-maximal dose level of TSH or noradrenaline. Furthermore, neither L-propranolol nor methylatropine influenced the GRP-induced thyroid hormone secretion. It is concluded that GRP has the capacity to stimulate basal thyroid hormone secretion in the mouse.