P77The effect of urotensin II on calcium regulation during excitation-contraction coupling

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Funding Acknowledgements: University of Basrah/Iraq Introduction: Heart failure is characterized by left ventricular dysfunction due to aberrant Ca2+-regulation during excitation-contraction (E-C) coupling. Plasma levels of UII is elevated in patients with heart failure, and me be related to dysfunction of Ca2+ hemostasis. The aim of this study is to investigate influence of UII on E-C coupling and Ca2+-regulation. Methods: The Langendorff perfused isolated rat heart was used to study effect of UII on left ventricular function. Adult Rat Ventricular Myocytes (ARVMs) were isolated from Wistar rats by enzymatic digestion. Percentage cell shortening of ARVMs was measured using the video-based edge detection system. Intracellular Ca2+ was measured in single freshly isolated ARVMs loaded with Fura-2 and sarcoplasmic reticulum Ca2+ content [Ca2+]SR was determined by rapid application of 10mM caffeine. Action potential was recorded using the whole cell patch clamp technique and resistance pipette value of the seal was (12-15MΩ). Results: Exposure of rat heart to 50nM UII Caused a 19.7 ± 2.5% reduction in left ventricular developed pressure (LVDP) (n = 8 hearts). The mechanical properties of ARVMs were assessed, the results show a significant reduction in the cell shortening from 12.6 ± 0.5% control to 10.9 ± 0.5% in UII-treated cells (n = 71 cells) (P<0.0001).

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