Electrical and chemical stimulation of cervical sympathetic nerves in the dog does not affect secretion of parathyroid hormone.
beta-Adrenergic agonists stimulate PTH release in vitro. The present studies were designed to test the hypothesis that norepinephrine released from sympathetic nerve terminals in the parathyroid glands might be a physiological regulator of PTH secretion. In 22 dogs, electrical stimulation (20 Hz, 1 msec, 50 V nominal) of the right cervical vagosympathetic trunk had no significant effect on release of PTH into the precava, whether the animals were normocalcemic or hypocalcemic, and whether or not they were pretreated with the alpha-adrenergic antagonist phenoxybenzamine. In 4 other dogs, stimulating release of endogenous nerve terminal norepinephrine by iv injection of tyramine (200 micrograms/kg) also failed to raise precaval plasma immunoreactive PTH concentrations. In all studies, induction of mild hypocalcemia raised immunoreactive PTH levels. From these and other studies, we conclude that beta-adrenergic agonists of neural origin are not important regulators of canine PTH release in vivo.
Heath
H
H
Fox
J
J
Fryer
M
M
Laakso
K
K
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001679:Biogenic Amines / Q000032:analysis; D004285:Dogs; D004533:Egtazic Acid / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D010280:Parathyroid Glands / Q000032:analysis; D010281:Parathyroid Hormone / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000502:physiology*; D014439:Tyramine / Q000494:pharmacology
D000318:Adrenergic beta-Agonists; D001679:Biogenic Amines; D010281:Parathyroid Hormone; D004533:Egtazic Acid; D014439:Tyramine