Stern J E, Cardinali D P
Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Biol Signals. 1994 Jan-Feb;3(1):15-25. doi: 10.1159/000109522.
The local surgical manipulation of sympathetic and parasympathetic nerves innervating the thyroid-parathyroid territory was employed to search for the existence of a peripheral neuroendocrine link controlling parathyroid hormone (PTH) and calcitonin (CT) release. From 8 to 24 h after superior cervical ganglionectomy (SCGx), at the time of wallerian degeneration of thyroid-parathyroid sympathetic nerve terminals, an alpha-adrenergic inhibition, together with a minor beta-adrenergic stimulation, of hypercalcemia-induced CT release, and an alpha-adrenoceptor inhibition of hypocalcemia-induced PTH release were found. In chronically SCGx rats PTH response to EDTA was slower, and after CaCl2 injection, serum calcium attained higher levels in face of normal CT levels. SCGx blocked the PTH increase found in sham-operated rats stressed by a subcutaneous injection of turpentine oil, but did not affect the greater response to EDTA. The higher hypocalcemia seen after turpentine oil was no longer observed in SCGx rats. The effects of turpentine oil stress on calcium and CT responses to a bolus injection of CaCl2 persisted in rats subjected to SCGx 14 days earlier. Interruption of thyroid-parathyroid parasympathetic input conveyed by the thyroid nerves (TN) and the inferior laryngeal nerves (ILN) caused a fall in total serum calcium, an increase of PTH levels and a decrease of CT levels, when measured 10 days after surgery. Greater responses of serum CT and PTH were detected in TN-sectioned, and in TN- or ILN-sectioned rats, respectively. Physiological concentrations of CT decreased, and those of PTH increased, in vitro cholinergic activity in rat SCG, measured as specific choline uptake, and acetylcholine synthesis and release. The results indicate that cervical autonomic nerves constitute a pathway through which the brain modulates calcium homeostasis.
通过对支配甲状腺 - 甲状旁腺区域的交感神经和副交感神经进行局部手术操作,来探寻控制甲状旁腺激素(PTH)和降钙素(CT)释放的外周神经内分泌联系是否存在。在颈上神经节切除术(SCGx)后8至24小时,即甲状腺 - 甲状旁腺交感神经末梢发生华勒氏变性时,发现高钙血症诱导的CT释放受到α - 肾上腺素能抑制以及轻微的β - 肾上腺素能刺激,而低钙血症诱导的PTH释放受到α - 肾上腺素能受体抑制。在慢性SCGx大鼠中,PTH对EDTA的反应较慢,并且在注射氯化钙后,面对正常的CT水平,血清钙达到更高水平。SCGx阻断了皮下注射松节油应激的假手术大鼠中出现的PTH升高,但不影响对EDTA的更大反应。在SCGx大鼠中不再观察到松节油注射后出现的更高程度的低钙血症。松节油应激对钙和CT对氯化钙推注的反应的影响在14天前接受SCGx的大鼠中仍然存在。在甲状腺神经(TN)和喉返神经(ILN)传递的甲状腺 - 甲状旁腺副交感神经输入中断后,在手术后10天测量时,总血清钙下降,PTH水平升高,CT水平下降。在分别切断TN以及切断TN或ILN的大鼠中检测到血清CT和PTH的更大反应。以特异性胆碱摄取、乙酰胆碱合成和释放来衡量,大鼠SCG中的体外胆碱能活性在生理浓度的CT降低时增加,而PTH的生理浓度增加。结果表明,颈自主神经构成了大脑调节钙稳态的一条途径。