2021-12

EsiTech 2021 International Conference on Sustainable Future and Environmental Science

Angiotensin II (Ang II) exerts numerous effects on the cardiovascular system including the regulation of blood pressure. The current study focused on the potential mechanisms that seem to be involved in the Ang II vasodilation using bovine aortic endothelial cell (BAE-1). Expression of Ang II receptor (AT2) in BAE-1 was checked by western blots in the presence of valsartan (AT1inhibitor). The vasodilator effect of Ang II was enhanced in the presence of valsartan in comparison with control; while being decreased in the presence of PD123177 (AT2 inhibitor). To examine whether the vasodilator effect of Ang II occurred through the nitric oxide (NO) pathway, the Griess reagent was used and the experimental data indicated that NO level increased in a concentration-dependent manner. Meanwhile, at Ang II at a concentration of 1 µM, the level of NO increased more than at 100 µM. In patch-clamp experiments, K current, and chord conductance were enhanced after incubation of Ang II with valsartan. When 100 µM Ang II was added, the current peaked rapidly in a time-dependent manner and reached a maximum value after 15 min of incubation as compared to 10 min and control. Ang II type two receptor inhibitor (PD1231777) reduced the current and conductance induced by Ang II. In conclusion, Ang II released NO via the activation of AT2. KCa currents were stimulated by Ang II and evoked mainly a current consistent with the activation of KCa channels.

2021-08

Second International Science Conference in Zakho University, Zakho , (2017)

Sodium Nitroprusside (SNP) and Adenosine (Ado) are potent drugs used in the treatment of cardiovascular diseases. Nitric oxid (NO) is produced from virtually all cell types composing the cardiovascular and regulates vascular function through fine regulation of excitation–contraction coupling. Adinosine endogenous metabolites play a major role in coronary autoregulation. Therefore, the aim of the present study was to investigate the contribution of NO and Ado mediated relaxation in rat aortic smooth muscle in intact and denuded endothelium rings precontracted with phenylepherine (PE). The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers and isometric tension was recorded using powerLab Data Acquisition System (Model ML 870). According to the results of the current study, incubation of aortic rings with Glybenclamide (GLIB) decreased the relaxation response induced by Ado (the vasodilation value rate decrease from 41.07±6.7 control to 18.54±4.6) in intact aortic rings. Lnitroarginine methylester (L-NAME), not abolished the response induced by SNP, whereas Nifedipine significantly enhanced the response induced by SNP in a dose-dependent manner in intact endothelium rings. The relaxation to Ado in intact aortic rings was slightly decreased (6.88± 1.01), but not abolished completely after incubation with Caffeine (Ado receptors antagonist). On the other hand, removing endothelium did not attenuated the vasorelaxation induced by SNP and increased relaxation response. While, vasorelaxation of Ado in aortic rings were partially attenuated by removing endothelium. These results suggested that (1) ATP-dependent potassium channel (KATP) did not involve in SNP inducing vasorelaxation, while have a role in Ado mediated vasorelation. (2) Vasorelaxation effect of NO is endothelium independent, while, Ado relaxation effect is endothelium dependent.

2021-08

First International Science Conference in Zakho University, Zakho , (2013)

Sodium Nitroprussid and Adenosine-Activated Potassium Channel in Aortic Smooth Muscle Isolated From Female Rats

2011-04

First International Science Conference in Zakho University, Zakho

Nitric oxide (NO) is produced from virtually all cell types composing the cardiovascular tissue and regulates vascular function through fine regulation of excitation–contraction coupling. Endogenous metabolites play a major role in coronary autoregulation. Therefore, the aim of the present study is to investigate the contribution of Glyceryl trinitrate (GTN) and Adenosine 5-triphosphate (ATP) mediated relaxation in rat aortic smooth muscle in intact and endothelium denuded endothelium rings precontracted with Phenylephrine (PE). The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers and isometric tension was recorded using PowerLab Data Acquisition System (Model ML 870). The results showed that GTN as NO donor produced dose-dependent relaxation in intact aortic rings precontracted with PE (1 µM) that disinhibited in the presence of Glibenclamide (GLIB), while GLIB attenuate the response induced by ATP in intact aortic rings. L-nitroarginine methylester (LNAME) an antagonist for nitric oxide synthases (NOS), not abolish the response induced by GTN (Emax 55.28% ± 0.18). Caffeine, ATP receptors antagonist, were partially inhibit the relaxation induced by ATP (vasodilation rate decreased by about 20.57 %). In endothelium denuded aortic rings, vasorelaxation induced by ATP were significantly attenuated , while GTN significantly increased relaxation by removing endothelium. These results suggested that (1) ATP-dependent potassium channel did not involve in GTN inducing vasorelaxation while KATP and A2B receptors have a role in ATP mediated vasorelation (2) ATP partially dependent on endothelium in contrast to NO donors that independent to endothelium.