Smooth Muscle–Specific Deletion of Nitric Oxide–Sensitive Guanylyl Cyclase Is Sufficient to Induce Hypertension in Mice | Zendy

Dieter Groneberg | Zendy; Peter König | Zendy; Angela Wirth | Zendy; Stefan Offermanns | Zendy; Doris Koesling | Zendy; Andreas Friebe | Zendy

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Smooth Muscle–Specific Deletion of Nitric Oxide–Sensitive Guanylyl Cyclase Is Sufficient to Induce Hypertension in Mice

Author(s) -

Dieter Groneberg,

Peter König,

Angela Wirth,

Stefan Offermanns,

Doris Koesling,

Andreas Friebe

Publication year - 2010

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.109.890962

Subject(s) - nitric oxide , medicine , transgene , endocrinology , knockout mouse , vascular smooth muscle , tamoxifen , soluble guanylyl cyclase , genetically modified mouse , receptor , guanylate cyclase , biology , smooth muscle , gene , biochemistry , cancer , breast cancer

Arterial hypertension is one of the major diseases in industrial countries and a major cause of mortality. One of the main vascular factors responsible for the relaxation of blood vessels and regulation of blood pressure is nitric oxide (NO). NO acts predominantly via NO-sensitive guanylyl cyclase (NO-GC), which is made up of 2 different subunits (alpha and beta). Deletion of the beta(1) subunit leads to a global NO-GC knockout, and these mice are hypertensive. However, global deletion of NO-GC in mice does not allow identification of the cell/tissue type responsible for the elevated blood pressure.

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