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We generated mice lacking Vhl in catecholaminergic cells. They exhibited atrophy of the carotid body (CB), adrenal medulla, and sympathetic ganglia.\n                    <jats:italic>Vhl<\/jats:italic>\n                    \u2010null animals had an increased number of adult CB stem cells, although the survival of newly generated neuron\u2010like glomus cells was severely compromised. The effects of Vhl deficiency were neither prevented by pharmacological inhibition of prolyl hydroxylases or selective genetic down\u2010regulation of prolyl hydroxylase\u20103, nor phenocopied by hypoxia inducible factor overexpression. Vhl\u2010deficient animals appeared normal in normoxia but survived for only a few days in hypoxia, presenting with pronounced erythrocytosis, pulmonary edema, and right cardiac hypertrophy. Therefore, in the normal sympathoadrenal setting,\n                    <jats:italic>Vhl<\/jats:italic>\n                    deletion does not give rise to tumors but impairs development and plasticity of the peripheral O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010sensing system required for survival in hypoxic conditions.\n                  <\/jats:p>","DOI":"10.15252\/emmm.201404153","type":"journal-article","created":{"date-parts":[[2014,11,10]],"date-time":"2014-11-10T23:29:22Z","timestamp":1415662162000},"page":"1577-1592","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["Deletion of the von Hippel\u2013Lindau gene causes sympathoadrenal cell death and impairs chemoreceptor\u2010mediated adaptation to hypoxia"],"prefix":"10.1038","volume":"6","author":[{"given":"David","family":"Mac\u00edas","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary Carmen","family":"Fern\u00e1ndez\u2010Ag\u00fcera","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria","family":"Bonilla\u2010Henao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9","family":"L\u00f3pez\u2010Barneo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2014,11,10]]},"reference":[{"key":"BFEMMM201404153_CR1","doi-asserted-by":"crossref","first-page":"614","DOI":"10.1038\/ng1019","volume":"32","author":"SO Ang","year":"2002","unstructured":"Ang SO, Chen H, Hirota K, Gordeuk VR, Jelinek J, Guan Y, Liu E, Sergueeva AI, Miasnikova GY, Mole D et\u00a0al (2002) Disruption of oxygen homeostasis underlies congenital Chuvash polycythemia. 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