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.