Some extracts:
About pain inhibition:
"Collectively, these data indicate that inosine is an agonist for A1Rs with antinociceptive properties and a potency similar to adenosine and can be considered another endogenous ligand for this receptor."
"Taken together, these data suggest that the antinociceptive effect of inosine is mediated,
in part, by pertussis toxin-sensitive G-protein coupled receptors and the subsequent activation of voltage gated K+ channel, large conductance Ca2+-activated and ATP-sensitive K+ channels or inactivation of voltage-gated Ca2+ channels.
Finally, small conductance Ca2+-activated K+ channels are not involved in the antinociceptive effect of inosine."
"It is well known that adenine-based
purines exert multiple effects on pain transmission. Recently, we have demonstrated that guanine-based purines may produce some
antinociceptive effects against chemical and thermal pain in mice.
These effects seem to be related, at least partially, to the modulation of A1 adenosine receptors."
About effect on Detrusor activity:
"Inosine is a naturally occurring purine nucleoside with neuroprotective, neurotrophic and antioxidant effects that is known to improve motor function in preclinical models of Spinal Cord Injury.
These findings demonstrate that inosine prevents the development of detrusor overactivity and attenuates existing overactivity following SCI, and may achieve its effects through modulation of sensory neurotransmission"
"Our results indicate that inosine treatment attenuated the injury-induced increase in TRPV1 immunoreactivity, both with immediate and delayed administration, in parallel with significant improvements in detrusor overactivity. Together, these findings suggest that inosine achieves its effects, at least in part, through inhibition of TRPV1 expression and/or activity."
"Inosine is also known to act through interaction with members of the adenosine receptor family [
24,
25,
26] For example, the anti-nociceptive effects of inosine in diverse models of pain were found to be mediated via A1 and A2A subtypes, resulting in inhibition of protein kinase C [
25] and protein kinase A, as well as modulation of KATP, Kv and BK channels [
26]. A2A receptor activation was also implicated in relaxation of bladder muscle strips via KATP activation and elevation of intracellular cAMP [
27], as well as in the immunosuppressive activity of inosine in experimental models of inflammation [
24]"
Our findings implicate A2B in mediating the beneficial inhibitory effect of inosine on spontaneous activity in tissues from rats with NDO. Interestingly, a recent report implicated A2B in adenosine-mediated relaxation of precontracted detrusor strips from the rat bladder
31. Together with observations that decreases in expression of the A2B receptor have been reported to contribute to a reduction in evoked detrusor relaxation with aging and with declining estrogens
30,
32, these findings emphasise the potential for inosine as a pharmacologic agonist of A2B as well as a strategy for modulating bladder activity."
"Inosine inhibits spontaneous activity in bladder tissue from SCI rats through a mechanism mediated by A2B adenosine receptors that impinges on large conductance BK channels"