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.