Effects Of angiotensin II and Telmisartan on transient outward potassium and L-type calcium currents in Sprague–Dawley rat atrial myocytes

Objective To explore possible electrophysiological mechanisms of single atrial myocyte by evaluating the effects of angiotensinII (AngII) and telmisartan on transient outward potassium currents (Ito) and L-type calcium currents (ICa-L) in Sprague–Dawley rats. Methods Single atrial myocyte of SD rats was obtained by enzymatic dissociation method. The whole cell patch-clamp recording technique was used to record the change of Ito and ICa-L by intervening of AngII, telmisartan and AngII plus telmisartan, respectively. Experimental groups: (1) AngII group: cells were perfused with bath solution containing AngII (0.1 μmol/l); (2) Telmisartan group: cells were perfused with bath solution containing telmisartan (0.01 μmol/l); (3) Combined group, myocytes were perfused with bath solution containing AngII (0.1 μmol/l) and telmisartan (0.01 μmol/l). Results Compared with baseline value, AngII (0.1μmol/l), Telmisartan (0.01 μmol/l) and AngII plus Telmisartan group significantly decreased the peak density of Ito in SD rat atrial myocytes (22.48±2.75 vs 15.71±2.06 pA/pF, p<0.01), (24.16±2.36 vs 16.15±1.82 pA/pF, p<0.01) and (24.41±2.27 vs 21.35±1.46 pA/pF, p<0.05), respectively. AngII (0.1 μmol/l) significantly increased the peak density of ICa-L in SD rat atrial myocytes (−4.51±0.38 vs −5.16±0.29 pA/pF, p<0.01). Telmisartan (0.01 μmol/l) had no significant effect on ICa-L in the rat atrial myocytes (−4.35±0.27 vs −4.29±0.34 pA/pF, p>0.05), but it could antagonise the effects of AngII. In the Ang IIcombined telmisartan group, the peak density of ICa-L was (−4.08±0.28 vs −4.20±0.31 pA/pF, p>0.05), which was significantly different from that of AngII group (p<0.05). Conclusion AngII and telmisartan had directly electrophysiological effects on SD rat atrial myocytes as well as telmisartan had antagonist effects on AngII at the level of angiotensin receptor.