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Zbucki, R.L., Dadan, I., Sawicki, B., Bialuk, I., Kosiozek, P., Winnicka, M. and Puchalski, Z. (2004) Propranolol Alters the Activity of Thyroid C-Cells in the Experimental Model of Hyperthyroidism in Rats. Proceedings of the 15 International Congress of the Polish Pharmacological Society, Poznan, 12-14 September 2004, 223.

has been cited by the following article:

• TITLE: Calcitonin Secretion under Insulin Hypoglycemia

  AUTHORS: Svetlana Stepanovna Moisa, Alexander Danilovich Nozdrachev

  KEYWORDS: Calcitonin, Insulin Hypoglycemia, Autonomic Nervous System, Glucocorticoids, Glucagon

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.4 No.11, November 4, 2014

  ABSTRACT: The increasing secretion of calcitonin and hypocalcemia under insulin hypoglycemia, induced with insulin injection (1 IU/100g), was established. Physiological mechanisms of the stimulating effect of insulin hypoglycemia on calcitonin secretion were studied in double-side adrenalectomized and pancreatectomized rats and under the blocking synaptic transmission in sympathetic ganglions or via peripheral cholino- and adreno-receptor structures. Insulin hypoglycemia didn’t expose the increasing secretion of calcitonin in rats under adrenalectomy and pancreatectomy. Ganglion-blocker pentamin (2.5 mg/100g body weight), blocker of M-cholino-receptors atropine (0.2 ml), α-adreno-blocker tropaphen (0.1 mg/100g), and β-adreno-blocker obzidan (0.1 mg/100g) evoked the inhibiting effect on calcitonin secretion in spite of simultaneously increasing of hypog-lycemia. Corticosteroids and, obviously, glucagon and also the tone of autonomic nervous system via peripheral M-cholinoreactive and α- and β-adrenoreactive structures take part in the activation of calcitonin secretion under insulin hypoglycemia.