Natriuretic peptide system expression in murine and human submandibular salivary glands: a study of the spatial localisation of ANB, BNP, CNP and their receptors

Abstract

The natriuretic peptide (NP) system comprises of three ligands, the Atrial Natriuretic Peptide (ANP), Brain Natriuretic peptide (BNP) and C-type Natriuretic peptide (CNP), and three natriuretic peptide receptors, NPRA, NPRB and NPRC. Here we present a comprehensive study of the natriuretic peptide system in healthy murine and human submandibular salivary glands (SMGs). We show CNP is the dominant NP in mouse and human SMG and is expressed together with NP receptors in ducts, autonomic nerves and the microvasculature of the gland, suggesting CNP autocrine signalling may take place in some of these glandular structures. These data suggest the NP system may control salivary gland function during homeostasis through the regulation of electrolyte re-absorption, neural stimulation and/or blood vessel wall contraction/relaxation. We also show abnormal expression of NPRA in the stroma of a subset of human SMGs resected from patients diagnosed with oral squamous cell carcinoma (OSCC) of non-salivary gland origin. This finding warrants further research to investigate a possible correlation between early OSCC invasion and NPRA overexpression.

Intradermal Administration of Atrial Natriuretic Peptide Attenuates Cutaneous Vasodilation but Not Sweating in Young Men during Exercise in the Heat

“…Local ANP administration did not influence thermoregulatory sweating during rest or exercise in the heat, which is consistent with our prior work demonstrating no modulating effect of exogenous ANP on cholinergic sweating under thermoneutral conditions [11]. Accordingly, although the membrane-bound receptor for ANP, GC-A, has been localized in cells of human exocrine glands, including eccrine sweat glands [41,42] and sympathetic cholinergic nerves innervating eccrine glands are immunoreactive to ANP [43], based on our combined studies it appears that this hormone exerts a negligible direct influence on human eccrine sweat gland function in vivo. However, it is still plausible that either intravascular ANP infusion or increased levels of endogenously derived ANP in the blood, as occurs during progressive dehydration during an exercise-induced heat stress [2,6], may influence thermoregulatory sweating under these conditions due to the complex regulatory effects of ANP on plasma volume and osmolality, which both modulate sweat output during exercise [12,13].…”