Altered Delayed Rectifier K<SUP>&#8290;</SUP> Current of Rabbit Coronary Arterial Myocytes in Isoproterenol-Induced Hypertrophy

Altered Delayed Rectifier K<SUP>&#8290;</SUP> Current of Rabbit Coronary Arterial Myocytes in Isoproterenol-Induced Hypertrophy

<P> The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier K<SUP>&#8290;</SUP> (K<SUB>DR</SUB>) channel function in isoproterenol-induced hypertrophy. It has been proposed that K<SUB>DR</SUB> channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary K<SUB>DR</SUB> channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary K<SUB>DR</SUB> channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the K<SUB>DR</SUB> current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary K<SUB>DR</SUB> channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of K<SUB>DR</SUB> channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.