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Deprecated: Implicit conversion from float 294.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Exp+Clin+Cardiol 2012 ; 17 (3): 89-94 Nephropedia Template TP
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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
Exp Clin Cardiol 2012[Sep]; 17 (3): 89-94 PMID23620694show 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+, Ca2+ 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 Ca2+-dependent NO release.