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Hypotension due to Kir6.1 gain-of-function in vascular smooth muscle.

Anlong Li | Russell H Knutsen | Haixia Zhang | Patrick Osei-Owusu | Alex Moreno-Dominguez | Theresa M Harter | Keita Uchida | Maria S Remedi | Hans H Dietrich | Carlos Bernal-Mizrachi | Kendall J Blumer | Robert P Mecham | Joseph C Koster | Colin G Nichols
Journal of the American Heart Association | 2013

KATP channels, assembled from pore-forming (Kir6.1 or Kir6.2) and regulatory (SUR1 or SUR2) subunits, link metabolism to excitability. Loss of Kir6.2 results in hypoglycemia and hyperinsulinemia, whereas loss of Kir6.1 causes Prinzmetal angina-like symptoms in mice. Conversely, overactivity of Kir6.2 induces neonatal diabetes in mice and humans, but consequences of Kir6.1 overactivity are unknown.

Pubmed ID: 23974906

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Associated grants

  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL045742
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS071011
  • Agency: NINDS NIH HHS, United States
    Id: NS071011
  • Agency: NHLBI NIH HHS, United States
    Id: HL45742
  • Agency: NHLBI NIH HHS, United States
    Id: HL041250
  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL041250
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK020579

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C57BL/6J (tool)

RRID:IMSR_JAX:000664

Mus musculus with name C57BL/6J from IMSR.

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