BK Influence On 20-HETE Induced Changes On Myocardial Mechanics On Rat

20-Hydroxyeicosatetraenoic acid (20-HETE) is anω-hydroxylated arachidonic acid (AA) metabolite. 20-HETE plays a important role the cardiovascular system like, a overexpression of 20-HETE plays an important role in the pathogenesis of hypertension.Bradykinin as know is a peptide that causes blood vessels to enlarge (dilate), and therefore causes blood pressure to lower. It's also a class of drugs called ACE inhibitors, which are used to lower blood pressure; it works on blood vessels through the release of Prostacyclin, nitric oxide, and endothelial-derived hyperpolarizing factor. Also Bradykinin is known as potent endothelium-dependent vasodilator, causes contraction of non-vascular smooth muscle, increases vascular permeability and also is involved in the mechanism of pain.Bradykinin has been demonstrated to have a cardioprotective role by affecting metabolic processes and tissue perfusion under conditions of myocardial ischemia and it's also have been demonstrated that CYPω-hydroxylases and their AA metabolite, 20-HETE, have a significant detrimental role in enhancing myocardial ischemia-reperfusion injury in rat heart.Some findings suggest that in isolated mouse hearts the BK-induced vasodilation is mediated by NO and CYP450 metabolites but not by prostaglandins. And It's also known that Bradykinin stimulate 20-HETE formation in the TALH.The present study was undertaken to establish the underlying mechanism(s) of influence of 20-HETE induced changes on myocardial mechanics on rat In Vivo and in Langendorff.We therefore explored the possibility that 20-HETE vasoconstriction may be mediate by Bradykinin to this end, we tested the effect of 20-HETE and BK on the hemodynamic parameters of wister rat weighting between 150 to 200 g. the In Vivo model of cardiac changes in myocardial mechanics (the right carotid catheterization) and the Langendorff procedure has been done to anchor these hemodynamic parameters recording throughout the experiment of PowerLab life science data acquisition system (Powerlab8.0, Australia). The hemodynamic parameter which include: the LVP (kPa), LVEDP (kPa), Heart rate (beat/min), LV dP/dtmax ( kPa/s) data were analyzed using chart 5Ch specially designed software (Powerlab8.0, Australia). In reperfused heart the LVSP changed with different doses of 20-HETE. In low dose (1-3 nM), 20-HETE has increase the LVSP and the dP/dt max and dP/dt min. in high dose (10 nM), 20-HETE decrease the LVSP of the reperfused rat heart. Only a high dose of 20-HETE (10 nM) showed an increased of the heart rate while low doses (1-3 nM) did not show a significant different with Control (Fig 7) .In the In Vivo myocardial mechanisms recording a bolus injection of 30 nM of BK showed a decrease of 19.81% in the LVSP (7.95±0.49 kPa) vs (8.51±0.57 kPa) for 20-HETE 3 nM. In reperfused heart myocardial recording a bolus injection of 30 nM of BK has shown a decrease of 11. 76% of the LVSP from 3.4 kPa (20-HETE 3 nM) to 3 kPa (BK 30 nM) (Fig 13).