No abstract

Nitrofurazone-impregnated urinary catheters reduced the incidence of CABF in adult trauma patients, reducing the need to change or prescribe new antimicrobial therapy. ClinicalTrials.gov registration number: NCT00192985.

Nitric oxide (NO) plays multiple roles in both intracellular and extracellular signalling mechanisms with implications for health and disease. This review focuses on the role of NO signalling in salivary secretion. Attention will be paid primarily to endogenous NO production in acinar cells resulting from specific receptor stimulation and to NO-regulated Ca2+ homeostasis. Due to the fact that NO readily crosses membranes by simple diffusion, endogenous NO may play a physiological role in processes as diverse as modifying the secretory output, controlling blood supply to the gland, modulating transmitter output from nerve endings, participating in the host defence barrier, and affecting growth and differentiation of surrounding tissue. Furthermore, the role of NO in the pathogenesis of human oral diseases will be considered.

We characterized the enzymic properties of ADP-ribosyl cyclase in rat parotid acinar cells by using a fluorescence technique. ADP-ribosyl cyclase is capable of synthesizing the Ca# + -mobilizing nucleotide cADP-ribose (cADPR) from NAD + and has previously been shown to be regulated by cGMP via a cGMP-dependent protein kinase (G kinase). We therefore investigated whether NO\cGMP-activated pathways are present in rat parotid acinar cells and whether NO\cGMP signalling exerts control over cellular Ca# + signalling processes. Our results showed that stimulation of acinar cells with adrenaline, isoproterenol, substance P and NO resulted in a rise in the [cGMP]. In addition, NO induced a release of Ca# + from intracellular ryanodine-

The activity of nitric oxide synthase (NOS) in rat parotid acinar cells was measured using a newly synthesized fluorescent NO indicator DAF-2/DA. Our results show that NO production is most effectively stimulated by activation of the beta-adrenergic receptor, and to a minor extent by substance P (SP). NO activates the production of cGMP, an intracellular messenger that has been shown to release Ca2+ from ryanodine-sensitive intracellular stores. We found that cGMP is also able to release Ca2+ from ryanodine-insensitive intracellular stores. Our data show that a rise in the cGMP concentration induces inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] synthesis and Ca2+ release from intracellular stores.