Low K+ current in arterial myocytes with impaired K+-vasodilation and its recovery by exercise in hypertensive rats

K + channels determine the plasma membrane potential of vascular myocytes, influencing arterial tone. In many types of arteries, a moderate increase in [K + ] e induces vasorelaxation by augmenting the inwardly rectifying K + channel current ( I Kir ). K + -vasodilation matches regional tissue activity and O 2 supply. In chronic hypertension (HT), small arteries and arterioles undergo various changes; however, ion channel remodeling is poorly understood. Here, we investigated whether K + channels and K + -induced vasodilation are affected in deep femoral (DFA) and cerebral artery (CA) myocytes of angiotensin II-induced hypertensive rats (Ang-HT). Additionally, we tested whether regular exercise training (ET) restores HT-associated changes in K + channel activity. In Ang-HT, both the voltage-gated K + channel current ( I Kv ) and I Kir were decreased in DFA and CA myocytes, and were effectively restored and further increased by combined ET for 2 weeks (HT-ET). Consistently, K + -vasodilation of the DFA was impaired in Ang-HT, and recovered in HT-ET. Interestingly, ET did not reverse the decreased K + -vasodilation of CA. CA myocytes from the Ang-HT and HT-ET groups demonstrated, apart from K + channel changes, an increase in nonselective cationic current ( I NSC ). In contrast, DFA myocytes exhibited decreased I NSC in both the Ang-HT and HT-ET groups. Taken together, the decreased K + conductance in Ang-HT rats and its recovery by ET suggest increased peripheral arterial resistance in HT and the anti-hypertensive effects of ET, respectively. In addition, the common upregulation of I NSC in the CA in the Ang-HT and HT-ET groups might imply a protective adaptation preventing excessive cerebral blood flow under HT and strenuous exercise.