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

Authors: Miki, T  Suzuki, M  Shibasaki, T  Uemura, H  Sato, T  Yamaguchi, K  Koseki, H  Iwanaga, T  Nakaya, H  Seino, S 
Citation: Miki T, etal., Nat Med. 2002 May;8(5):466-72.
Pubmed: (View Article at PubMed) PMID:11984590
DOI: Full-text: DOI:10.1038/nm0502-466

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.

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RGD Object Information
RGD ID: 1581700
Created: 2006-10-19
Species: All species
Last Modified: 2006-10-19
Status: ACTIVE



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