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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Exp+Clin+Cardiol
2012 ; 17
(3
): 89-94
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Role of the transient receptor potential vanilloid type 1 receptor and
stretch-activated ion channels in nitric oxide release from endothelial cells of
the aorta and heart in rats
#MMPMID23620694
Torres-Narváez JC
; Mondragón Ldel V
; Varela López E
; Pérez-Torres I
; Díaz Juárez JA
; Suárez J
; Hernández GP
Exp Clin Cardiol
2012[Sep]; 17
(3
): 89-94
PMID23620694
show ga
Shear stress stimulates nitric oxide (NO) release in endothelial cells.
Stretch-activated ion channels (SACs) and the transient receptor potential
vanilloid type 1 (TRPV1) receptor respond to mechanical stimulus and are
permeable to Na(+), Ca(2+) and K(+). The influence of SACs and the TRPV1 receptor
on NO release on the heart and on the vascular reactivity of the thoracic aorta
(TA) was studied. Experiments were performed in isolated perfused heart, cultured
endothelial cells and TA rings from Wistar rats. Capsaicin (10 ?M, 30 ?M) was
used as a NO release stimulator, capsazepine (6 ?M, 10 ?M) was used as a
capsaicin antagonist and gadolinium (3 ?M, 5 ?M) was used as an inhibitor of
SACs. NO was measured by the Kelm and Tenorio methods. Left ventricular pressure
was recorded and coronary vascular resistance was calculated. Capsaicin increased
NO release in the heart by 58% (395±8 pmol/mL to 627±23 pmol/mL). Capsazepine and
gadolinium inhibited NO release by 74% and 82%, respectively. This tendency was
similar in all experimental models. Capsaicin attenuated the effects of
norepinephrine (10 M to 7 M) on TA and had no effect in the presence of N
(?)-nitro-L-arginine methyl ester. Therefore, the authors conclude that SACs and
the TRPV1 receptor are both present in the coronary endothelium and that both
participate in Ca(2+)-dependent NO release.