Induction of NADPH-diaphorase activity in the rat periaqueductal gray matter after nociceptive visceral stimulation

Role of nitric oxide in gastric motor and sensory functions in healthy subjects

“…This may be explained by the knowledge that NO has been shown to be mainly involved in the perception of visceral pain. 18 19 30 33 The healthy volunteers in our study predominantly reported bloating and satiation on gastric distension, rather than pain. One might however anticipate that NO synthase inhibition may have an effect on perception in dyspeptic patients with visceral hypersensitivity.…”

“…[11][12][13][14][15][16][17] In addition, evidence is available that NO is involved in the modulation of visceral perception, for example from rat experiments, showing that intraperitoneal injection of acetic acid results in an increase in nitrergic neurones in specific regions of the brain. 18 Also, NO synthase immune reactivity has been demonstrated in lumbosacral afferents and preganglionic neurones innervating the pelvic viscera. 19 Data illustrating a role for NO in human proximal gastric motility and perception are limited to in vitro studies 10 or to in vivo studies investigating the effect of NO donors such as nitrates.…”

Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats

“…NO immunoreactivity is associated with the nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) enzyme, which serves as a histochemical marker for neurons that produce NO [26]. A significant increase in NADPH-d-positive neurons in PAG was observed after noxious visceral stimulation, and a decrease in these neurons was observed after acupuncture in streptozotocin-induced diabetic rats [27,28]. Some investigators have also reported that NOS inhibition augments morphine-induced analgesia in experimental animals [29].…”

Relevance of nitric oxide in pain mechanisms and pain management

“…NO seems to represent the most important mediator of this phenomenon [3]. The role of NO as a neuronal messenger involved in processing of nociceptive transmission was also confirmed in rat studies in which neuronal NOS activity was significantly increased in the ventrolateral areas of the periaqueductal gray matter (PAG, a major pain sensitive center in the brain) after nociceptive visceral stimulation [4]. The electrical stimulation of dorsolateral PAG produces well-known hypertensive and analgesic effects, which are attenuated by serotonin.…”

“…The intrathecal administration of the NOS inhibitor (L-NAME) produced selective spinal inhibition of NOS and prevented the hyperalgesic response in a rat model of peripheral neuropathy. Intrathecal and intracerebroventricular administration of the selective inhibitor of NO-sensitive guanyl cyclase, (1-H- [1,2,4]oxadiazalo[4,3-a]quinoxalin-1-one, also decreased the hyperalgesic response to thermal stimuli [12]. In a chronic pain model in the rat (local injection of formalin into the hindpaw), L-NAME reduced licking behavior and Fos-labeling in the ipsilateral dorsal gray matter [13].…”