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Purpose : To determine the mechanism of vasorelaxant effect of 1-trifluoromethoxyphenyl – 3 -(1-propionylpiperidin–4-yl) urea (TPPU) in cardiovascular diseases, including hypertension. Methods : Isolated rat thoracic aortic tissue preparations were mounted in an organ bath set up integrated with isometric transducer and a Power Lab assembly. TPPU (0.3 - 100 μM) was tested for vasorelaxant effect against low K + (25 mM) and high K + (80 mM)-induced contractions and its mechanism was determined in the presence of different antagonists (glibenclamide, 4- aminopyridine and tetraethyl ammonium). Results : In rat aortic preparations, TPPU showed a concentration-dependent (0.3 – 100 μM) and significant (p < 0.001) inhibition of low K + induced contractions with complete inhibition obtained at 100 μM. TPPU produced significant (p < 0.05) inhibition of high K +  induced contractions with maximum relaxation of 15.36 ± 1.95 % and 15.85 ± 3.35 % at 30 and 100 μM, respectively. Glibenclamide (Gb,10 μM) pretreatment partially inhibited the vasorelaxant effect of TPPU against low K + in a concentration range of 1 - 30 μM. 4-Aminopyridine (4-AP, 1 mM) and tetraethyl ammonium (TEA, 10 mM), markedly inhibited the vasorelexant effect of TPPU against low K + induced contractions with maximum relaxation of 20.09 ± 2.40 and 21.67 ± 0.88 %, respectively, at 100 μM. Conclusion : TPPU possesses marked vasorelaxant properties which provides sound pharmacological evidence for its use as a potential drug candidate in the management of hypertension. Keywords : 1-Trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea, Hypertension, vasodilator, K+- channel activation, Ca+- channel antagonist

tropical journal of pharmaceutical research

Vasodilator effect of 1-trifluoromethoxyphenyl-3-(1- propionylpiperidin-4-yl) urea is predominantly mediated through activation of voltage-dependent K+ channels