ABSTRACT
<p><b>AIM</b>To study the effects of oxyphenamone (Oxy) on activation of Ca(2+)-activated K+ channels in rabbit mesenteric vascular smooth muscle cells.</p><p><b>METHODS</b>To measure the effect of Oxy on the Ca(2+)-activated K+ channel (BK (Ca) channel) activity in rabbit mesenteric vascular smooth muscle cells by using whole cell patch clamp techniques.</p><p><b>RESULTS</b>Oxy reversibly increase BK (Ca) channel activity in rabbit mesenteric artery smooth muscle cells. Application of Oxy (0.1 mumol.L-1) to the perfusion solution caused significant increase in outward currents and its effect was completely abolished by washout; The outward currents K+ was inhibited by TEA (7.5 mmol.L-1); Oxy activated the BK (Ca) channel in a dose-dependent manner (0.01-10 mumol.L-1).</p><p><b>CONCLUSION</b>Oxy directly increase the activity of BK (Ca) channel activity in rabbit mesenteric vascular smooth muscle cells in dose-dependent manner.</p>
Subject(s)
Animals , Rabbits , Cardiotonic Agents , Pharmacology , Mesenteric Arteries , Cell Biology , Muscle, Smooth, Vascular , Cell Biology , Myocytes, Smooth Muscle , Physiology , Organic Chemicals , Patch-Clamp Techniques , Potassium Channels, Calcium-ActivatedABSTRACT
<p><b>AIM</b>To study the vasorelaxation action of oxyphenamone (Oxy) and its mechanism.</p><p><b>METHODS</b>The contractile response of isolated rabbit renal, femoral and mesentery artery preparations was determined.</p><p><b>RESULTS</b>Oxy was shown to inhibit the contractile force of renal, femoral and mesentery arteries induced by phenylephrine in a concentration dependent manner. The vasorelaxation produced by Oxy was not attenuated by removal of the endothelium. Oxy (10(-6)-10(-4) mol.L-1) relaxed the contractions induced by KCl 30 mmol.L-1 as well as KCl 80 mmol.L-1, but the contraction curve of KCl 80 mmol.L-1 was shifted significantly to the right. Oxy in lower concentration (10(-6) and 5 x 10(-6) mol.L-1) increased the contractions induced by Ang II, and in middle concentration (10(-5) mol.L-1) it did not affect the contractions induced by Ang II. Whereas in higher concentration (5 x 10(-5) mol.L-1) it obviously inhibited the contractions induced by Ang II.</p><p><b>CONCLUSION</b>Oxy showed significant vasorelaxation to various vascular preparations, and its vasorelaxation action is endothelium independent. The mechanism of its vasorelaxations seems to be related with Ca2+ activated K+ channel (Kca channel) and Ca2+ channel in vascular smooth muscle cells but its true mechanism needs further study.</p>