摘要
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.
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.
