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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1.

The inwardly rectifying K(+) channel Kir6.1 forms K(+) channels by coupling with a sulfonylurea receptor in reconstituted systems, but the physiological roles of Kir6.1-containing K(+) channels have not been determined. We report here that mice lacking the gene encoding Kir6.1 (known as Kcnj8) have a high rate of sudden death associated with spontaneous ST elevation followed by atrioventricular block as seen on an electrocardiogram. The K(+) channel opener pinacidil did not induce K(+) currents in vascular smooth-muscle cells of Kir6.1-null mice, and there was no vasodilation response to pinacidil. The administration of methylergometrine, a vasoconstrictive agent, elicited ST elevation followed by cardiac death in Kir6.1-null mice but not in wild-type mice, indicating a phenotype characterized by hypercontractility of coronary arteries and resembling Prinzmetal (or variant) angina in humans. The Kir6.1-containing K(+) channel is critical in the regulation of vascular tonus, especially in the coronary arteries, and its disruption may cause Prinzmetal angina.[1]

References

  1. Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1. Miki, T., Suzuki, M., Shibasaki, T., Uemura, H., Sato, T., Yamaguchi, K., Koseki, H., Iwanaga, T., Nakaya, H., Seino, S. Nat. Med. (2002) [Pubmed]
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