Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
 free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 free
 free
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Anandamide elicits an acute release of nitric oxide through endothelial TRPV1 receptor activation in the rat arterial mesenteric bed Poblete IM; Orliac ML; Briones R; Adler-Graschinsky E; Huidobro-Toro JPJ Physiol 2005[Oct]; 568 (Pt 2): 539-51In the isolated rat mesenteric bed, the 1 min perfusion with 100 nm anandamide, a concentration that did not evoke vasorelaxation, elicited an acute release of 165.1 +/- 9.2 pmol nitric oxide (NO) that was paralleled by a 2-fold increase in cGMP tissue levels. The rise in NO released was mimicked by either (R)-(+)-methanandamide or the vanilloid receptor agonists resiniferatoxin and (E)-capsaicin but not by its inactive cis-isomer (Z)-capsaicin. The NO release elicited by either anandamide or capsaicin was reduced by the TRPV1 receptor antagonists 5'-iodoresiniferatoxin, SB 366791 and capsazepine as well as by the cannabinoid CB(1) receptor antagonists SR 141716A or AM251. The outflow of NO elicited by anandamide and capsaicin was also reduced by endothelium removal or NO synthase inhibition, suggesting the specific participation of endothelial TRPV1 receptors, rather than the novel endothelial TRPV4 receptors. Consistently, RT-PCR showed the expression of the mRNA coding for the rat TRPV1 receptor in the endothelial cell layer, in addition to its expression in sensory nerves. The participation of sensory nerves on the release of NO was precluded on the basis that neonatal denervation of the myenteric plexus sensory nerves did not modify the pattern of NO release induced by anandamide and capsaicin. We propose that low concentrations of anandamide, devoid of vasorelaxing effects, elicit an acute release of NO mediated predominantly by the activation of endothelial TRPV1 receptors whose physiological significance remains elusive.|Anilides/pharmacology[MESH]|Animals[MESH]|Arachidonic Acids/*pharmacology[MESH]|Cannabinoid Receptor Antagonists[MESH]|Capsaicin/analogs & derivatives/pharmacology[MESH]|Cinnamates/pharmacology[MESH]|Cyclic GMP/metabolism[MESH]|Diterpenes/pharmacology[MESH]|Dose-Response Relationship, Drug[MESH]|Endocannabinoids[MESH]|Endothelium, Vascular/*drug effects/metabolism[MESH]|In Vitro Techniques[MESH]|Male[MESH]|Mesenteric Artery, Superior/*drug effects/metabolism[MESH]|Nitric Oxide/metabolism[MESH]|Nitroarginine/pharmacology[MESH]|Perfusion[MESH]|Piperidines/pharmacology[MESH]|Polyunsaturated Alkamides[MESH]|Pyrazoles/pharmacology[MESH]|RNA, Messenger/analysis[MESH]|Rats[MESH]|Rats, Sprague-Dawley[MESH]|Rimonabant[MESH]|TRPV Cation Channels/*drug effects/genetics/metabolism[MESH]|Vasodilation/drug effects[MESH] |
