title: Low K⁺ current in arterial myocytes with impaired K⁺-vasodilation and its recovery by exercise in hypertensive rats.
abstract: 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 O2 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.
authors.affiliation: Department of Physiology, Department of Biomedical Sciences, and Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Daehak-Ro 103, Jongro-Gu, Seoul, 110-799, South Korea.
authors.forename: Eun Yeong
authors.initials: EY
authors.lastname: Seo
authors.forename: Hae Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Zai Hao
authors.initials: ZH
authors.lastname: Zhao
authors.forename: Ji Hyun
authors.initials: JH
authors.lastname: Jang
authors.forename: Chun Zi
authors.initials: CZ
authors.lastname: Jin
authors.forename: Hae Young
authors.initials: HY
authors.lastname: Yoo
authors.forename: Yin-Hua
authors.initials: YH
authors.lastname: Zhang
authors.forename: Sung Joon
authors.initials: SJ
authors.lastname: Kim
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001158:Arteries / Q000378:metabolism* / Q000503:physiopathology; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D032342:Muscle Cells / Q000378:metabolism* / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D024642:Potassium Channels, Voltage-Gated / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation / Q000502:physiology*
chemical_list: D024642:Potassium Channels, Voltage-Gated; D000804:Angiotensin II; D011188:Potassium