Piedras-Rentería E S, Sherwood O D, Best P M
Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana 61801, USA.
Am J Physiol. 1997 Apr;272(4 Pt 2):H1791-7. doi: 10.1152/ajpheart.1997.272.4.H1791.
The peptide hormone relaxin has direct, positive inotropic and chronotropic effects on rat hearts in vivo and in vitro. Relaxin's effects on the electrophysiological properties of single quiescent atrial cells from normal rats were investigated with a whole cell patch clamp. Relaxin had a significant inhibitory effect on outward potassium currents. The outward potassium current consisted of a transient component (I(to)) and a sustained component (I(S)). The addition of 100 ng/ml of relaxin inhibited the peak I(to) in a voltage-dependent manner (74% inhibition at a membrane potential of -10 mV to 30% inhibition at +70 mV). The time to reach peak I(to) and the apparent time constant of inactivation of I(to) were increased by relaxin. Dialysis with the protein kinase A inhibitor 5-24 amide (2 microM) prevented relaxin's effects, suggesting an obligatory role for this kinase in the relaxin-dependent regulation of the potassium current.
肽类激素松弛素在体内和体外对大鼠心脏具有直接的正性变力和变时作用。采用全细胞膜片钳技术研究了松弛素对正常大鼠单个静态心房细胞电生理特性的影响。松弛素对外向钾电流有显著抑制作用。外向钾电流由一个瞬时成分（I(to)）和一个持续成分（I(S)）组成。加入100 ng/ml的松弛素以电压依赖性方式抑制I(to)峰值（在膜电位为-10 mV时抑制74%，在+70 mV时抑制30%）。松弛素使达到I(to)峰值的时间和I(to)失活的表观时间常数增加。用蛋白激酶A抑制剂5-24酰胺（2 microM）进行透析可阻止松弛素的作用，提示该激酶在松弛素依赖性钾电流调节中起必要作用。
