Ca2+-conducting currents in parathyroid cells are modulated by muscarinic receptor agonists and antagonists.. Chang, Wenhan, Tsui-Hua Chen, Stacy A. Pratt, Benedict Yen, Michael Fu, Dolores Shoback[acute]i. Endocrine Research Unit, Departments of Medicine and Pathology, Veterans Affairs Medical Center, University of California, San Francisco, CA, 94121 and Wallenberg Laboratory, Goteborgs University, Gothenburg, Sweden.
APStracts 4:0155E, 1997.
Parathyroid cells express Ca2+-conducting cation currents in parathyroid cells, which are activated by raising extracellular [Ca2+] ([Ca2+]o) and blocked by dihydropyridines. We have found that acetylcholine (ACh) inhibited these currents in a reversible, dose -dependent manner (EC50 10-8 M). The inhibitory effects could be mimicked by the agonist (+)-muscarine. The effects of ACh were blunted by the antagonist atropine and reversed by removing ATP from the pipette solution. (+)-muscarine enhanced the cAMP production by 30%, but had no effects on inositol phosphate accumulation in parathyroid cells. Oligonucleotide primers, based on sequences of known muscarinic receptors (M1-M5), were used in reverse -transcriptase polymerase chain reaction (RT-PCR) to amplify receptor cDNA from parathyroid poly (A)+ RNA. RT-PCR products displayed > 90% nucleotide sequence identity to human M2 and M4 receptor cDNAs. Expression of M2 receptor protein was further confirmed by immunoblotting and immunocytochemistry. Thus, parathyroid cells express muscarinic receptors of M2 and possibly M4 subtypes. These receptor(s) may couple to dihydropyridine-sensitive cation-selective currents through the activation of adenylate cyclase and ATP -dependent pathways in these cells. 

Received 4 December 1996; accepted in final form 7 July 1997.
APS Manuscript Number E600-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 24 July 1997