Sympathetic innervation stimulates β-adrenergic receptors, triggering cyclic adenosine monophosphate (cAMP) production and enhancing protein secretion in salivary gland cells. While cAMP signaling, in conjunction with Ca2+ signaling, is essential for salivary gland function, the identified cAMP-producing G-protein-coupled receptors (GPCRs) remains limited. Here, we report the presence of cAMP-producing adenosine receptors in salivary gland cells. By reanalyzing publicly available single-cell transcriptome datasets of human and mouse submandibular glands, we identified mRNA expression of adenosine A1, A2A, A2B, and A3 receptors. Additionally, we confirmed that 5’-N-ethylcarboxamidoadenosine (NECA), an adenosine A2B receptor agonist, increases cAMP levels in human salivary gland cells, suggesting a physiological role for adenosine A2B receptors. Our findings enhance understanding of adenosine’s regulatory function in salivary glands and highlight new avenues for research on cAMPproducing adenosine receptors.

Keeping the intact germinal vesicle (GV) is essential for maintaining the capacity of mammals including human. It is maintained by very complex procedures along with folliculogenesis and is a critical step for getting competent oocyte. So far, a few mechanisms involved in folliculogenesis are known but GV arrest mechanisms are largely unrevealed. Cyclic AMP, a adenosine derived substance, have been used as inhibitor of germinal vesicle breakdown as a putative oocyte maturation inhibitor. In this study, we examined the potency of adenosine as GV maintainer and a possible signaling mediator for that. A1, A2b, and A3 were detected in cumulus cells of cumulus enclosed-oocyte (CEO). Intact of germinal vesicle was not kept like in follicle but the spontaneous maturation was inhibited by exogenous adenosine. It is inhibited with concentration dependent manners. Intracellular calcium level of cumulus was extensively increased after adenosine treatment. Based on these results it is suggested that one of the pathway for GV arrest by adenosine and its receptors is calcium mediated signaling pathway in CEO.