Basal nitric oxide limits immune, nervous and cardiovascular excitation: human endothelia express a mu opiate receptor

cis- and trans-acting elements involved in regulation of norB (norZ), the gene encoding nitric oxide reductase in Neisseria gonorrhoeae

“…In mice and humans, NO has also been shown to be an important modulator of the cellular events that form the immune response. Low basal levels of NO are anti-inflammatory, while high levels of NO, generated by inducible nitric oxide synthase (iNOS), are pro-inflammatory (Stefano et al, 2000;Davis et al, 2001). It has previously been shown that the ability of Neisseria meningitidis to detoxify NO has several implications when studied in a human macrophage model; NO reduction results in modulation of the resulting cytokine response, enhanced intracellular survival and inhibition of macrophage apoptosis (Stevanin et al, 2005Tunbridge et al, 2006).…”

Constitutive nitric oxide acting as a possible intercellular signaling molecule in the initiation of radiation-induced DNA double strand breaks in non-irradiated bystander cells

“…There are two principal pathways for the generation of NO after stimulation of the cells with chemicals or radiation, that is, by activation of iNOS or cNOS. Distinguishing the two forms of NOS are based on the activation time after the stimuli, the quantity of the NO generated and whether it is Ca 2 þ dependent or not (reviewed by Stefano et al, 2000). For constitutive NO , although the release level is only in the nM range, its transient release can have profound physiological activations for a longer period of time after NO has returned to its basal level (reviewed by Stefano et al, 2000).…”

“…Distinguishing the two forms of NOS are based on the activation time after the stimuli, the quantity of the NO generated and whether it is Ca 2 þ dependent or not (reviewed by Stefano et al, 2000). For constitutive NO , although the release level is only in the nM range, its transient release can have profound physiological activations for a longer period of time after NO has returned to its basal level (reviewed by Stefano et al, 2000). Stefano et al demonstrated that the release of NO from human endothelial cells treated with morphine or anandamide peaked within 5 min and returned to basal levels within 10 min.…”

“…Concurrently, the kinetics of NO production in the medium of irradiated cells after irradiation was rapid and in a timedependent manner as well, with a maximum yield observed at 10 min after irradiation with electron spin resonance analysis. Furthermore, our results that 7-Nitroindazole and L-NNA, but not aminoguanidine hemisulfate, treatment before exposure to 1 cGy a-particle significantly decrease the DIA of the conditioned medium suggested that constitutive NO from the irradiated cells possibly acted as an intercellular signaling molecule to initiate and activate the early process (p30 min) of bystanderIntroduction Nitric oxide (NO ), generated from arginine by the activation of nitric oxide synthase (NOS), is a major signaling molecule in the immune, cardiovascular and nervous systems (reviewed by Stefano et al, 2000), either by acting within the cell in which it is produced or by penetrating cell membranes to affect adjacent cells (Murad, 1998). The uniqueness of NO as a redox signaling molecule resides in part in its relative stability and hydrophobic properties that permit its diffusion through the cytoplasm and plasma membranes over several cell diameter distances (Beckman and Koppenol, 1996).…”

Estrogen and Morphine Modulate Their Own and the Other's Human Endothelial Receptor Expression via Nitric Oxide

“…Pharmacologic and immunologic evidence suggests that NO-coupled -subtype opiate receptors are expressed in human vascular endothelium [4,[6][7][8][9][10][11][12][13]. Using primers derived from the human neuronal 1 opiate receptor, we used RT-PCR to detect expression of  transcripts from human endothelia [4].…”