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

• Published in: Pflügers Archiv Vol. 466; no. 11; pp. 2101 - 2111
• Main Authors: Seo, Eun Yeong, Kim, Hae Jin, Zhao, Zai Hao, Jang, Ji Hyun, Jin, Chun Zi, Yoo, Hae Young, Zhang, Yin-Hua, Kim, Sung Joon
• Format: Journal Article
• Language: English
• Published: 01.11.2014
• ISSN: 0031-6768; 1432-2013
• DOI: 10.1007/s00424-014-1473-7

K super(+) channels determine the plasma membrane potential of vascular myocytes, influencing arterial tone. In many types of arteries, a moderate increase in [K super(+)] sub(e) induces vasorelaxation by augmenting the inwardly rectifying K super(+) channel current (I sub(Kir)). K super(+)-vasodilation matches regional tissue activity and O sub(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 super(+) channels and K super(+)-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 super(+) channel activity. In Ang-HT, both the voltage-gated K super(+) channel current (I sub(Kv)) and I sub(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 super(+)-vasodilation of the DFA was impaired in Ang-HT, and recovered in HT-ET. Interestingly, ET did not reverse the decreased K super(+)-vasodilation of CA. CA myocytes from the Ang-HT and HT-ET groups demonstrated, apart from K super(+) channel changes, an increase in nonselective cationic current (I sub(NSC)). In contrast, DFA myocytes exhibited decreased I sub(NSC) in both the Ang-HT and HT-ET groups. Taken together, the decreased K super(+) 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 sub(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.