beta-NAD is a novel nucleotide released on stimulation of nerve terminals in human urinary bladder detrusor muscle.

@article{Breen2006betaNADIA,
  title={beta-NAD is a novel nucleotide released on stimulation of nerve terminals in human urinary bladder detrusor muscle.},
  author={Leanne T Breen and Lisa M. Smyth and Ilia A. Yamboliev and Violeta N Mutafova-Yambolieva},
  journal={American journal of physiology. Renal physiology},
  year={2006},
  volume={290 2},
  pages={
          F486-95
        }
}
Endogenous nucleotides with extracellular functions may be involved in the complex neural control of human urinary bladder (HUB). Using HPLC techniques with fluorescence detection, we observed that in addition to ATP and its metabolites ADP, AMP and adenosine, electrical field stimulation (EFS; 4-16 Hz, 0.1 ms, 15 V, 60 s) of HUB detrusor smooth muscle coreleases novel nucleotide factors, which produce etheno-1N(6)-ADP-ribose (eADPR) on etheno-derivatization at high temperature. A detailed HPLC… 
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40 Citations
Background Citations
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Methods Citations
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Results Citations
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40 Citations

Neuronal and extraneuronal release of ATP and NAD+ in smooth muscle
TLDR
The purine hypothesis of neural regulation in smooth muscle is in need of reevaluation with emphasis on the roles of extracellular ATP and NAD+ and, further, will discuss more recent information about the likely involvement of multiple purines in Smooth muscle neurotransmission.
Storage and secretion of β‐NAD, ATP and dopamine in NGF‐differentiated rat pheochromocytoma PC12 cells
TLDR
Subcellular fractionation by continuous glycerol and sucrose gradients along with immunoblot analysis of the vesicular marker proteins synaptophysin and secretogranin II revealed that β‐NAD, ATP and DA are stored in both small synaptic‐like vesicles and large dense‐core‐likeVesicles, however, the three substances appear to have different preferential sites of release upon membrane depolarization.
Purinergic-Dependent Ca 2+ Pathways in Rat Pulmonary Artery Smooth Muscle Cells
TLDR
ADPR elicited concentration-dependent increase in [Ca 2+ ] i with a fast transient and a sustained phase in PASMCs, and the pharmacological profile of ATP-induced Ca 2+ response was distinctive from that of ADPR.
Effects of exogenous nicotinamide adenine dinucleotide (NAD+) in the rat heart are mediated by P2 purine receptors
TLDR
Extracellular NAD+ is supposed to be a novel regulator of cardiac electrical activity and P2 receptors represent the main target of NAD+ at least in the rat heart.
β-nicotinamide adenine dinucleotide is an enteric inhibitory neurotransmitter in human and nonhuman primate colons.
TLDR
β-NAD meets the criteria for a neurotransmitter better than ATP in human and monkey colons and therefore may contribute to neural regulation of colonic motility.
Release, neuronal effects and removal of extracellular β‐nicotinamide adenine dinucleotide (β‐NAD+) in the rat brain
TLDR
Rat brain synaptosomes can actively release, degrade and uptake β‐NAD+, and β‐ NAD+ can stimulate postsynaptic neurons, all criteria needed for a substance to be considered a candidate neurotransmitter in the brain.
N-type and P/Q-type calcium channels regulate differentially the release of noradrenaline, ATP and β-NAD in blood vessels
Novel localization of CD38 in perivascular sympathetic nerve terminals
Extracellular ATP and β-NAD alter electrical properties and cholinergic effects in the rat heart in age-specific manner
TLDR
The ability of ATP and β-NAD to alter cholinergic effects in the heart is estimated to be at the postsynaptic and presynaptic levels via affecting the cardiac myocytes APs and ACh release.
Cyclic ADP‐ribose requires CD38 to regulate the release of ATP in visceral smooth muscle
TLDR
Extracellular cADPR enhances the spontaneous release of ATP in the bladder by influx via CD38 and subsequent activation of intracellular cadPR receptors, probably causing an increase in intrace cellular Ca2+ in neuronal cells.
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