Rheumatology Medical News about Sjogren's syndrome;nitric oxide-mediated glandular hypofunction;non-apoptotic model

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A role for nitric oxide-mediated glandular hypofunction in a non-apoptotic model for Sjögren's syndrome
Rheumatology, 05/12/09

Caulfield VL et al. – Data show that chronic exposure to nitric oxide (NO), which is known to be elevated in Sjögren's syndrome (SS), could have a role in salivary gland hypofunction. NO-mediated nitrosylation of one or more elements of the signal transduction pathway could underlie down-regulation of salivary function in SS.

Methods

Aim was to investigate the role for the inflammatory mediator, NO in SS
FURA-2 microfluorimetry was used to measure agonist-evoked changes of Ca²⁺ in isolated mouse and human salivary acinar cells following exposure to NO donors

Results

NO had a biphasic effect on salivary acinar function
Acute exposure to NO (2 min) caused a cyclic GMP-dependent, 1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-sensitive increase in the Ca²⁺signal elicited in response to acetylcholine (ACh) stimulation
This was consistent with stimulation of ryanodine receptors by cyclic adenosine diphosphate ribose
Prolonged exposure to NO (>40 min) reduced the ACh-evoked Ca²⁺ signal by a mechanism independent of cyclic GMP
No differences between the responses of human and mouse acinar cells was noted

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