{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:04:42Z","timestamp":1774325082488,"version":"3.50.1"},"reference-count":48,"publisher":"Proceedings of the National Academy of Sciences","issue":"5","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2001,2,27]]},"abstract":"<jats:p>\n            Tissue kallikrein is a serine protease thought to be involved in\n the generation of bioactive peptide kinins in many organs like the\n kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal\n synthesis and urinary excretion of tissue kallikrein have been\n repeatedly linked to hypertension in animals and humans, but the exact\n role of the protease in cardiovascular function has not been\n established largely because of the lack of specific inhibitors. This\n study demonstrates that mice lacking tissue kallikrein are unable to\n generate significant levels of kinins in most tissues and develop\n cardiovascular abnormalities early in adulthood despite normal blood\n pressure. The heart exhibits septum and posterior wall thinning and a\n tendency to dilatation resulting in reduced left ventricular mass.\n Cardiac function estimated\n            <jats:italic>in vivo<\/jats:italic>\n            and\n            <jats:italic>in\n vitro<\/jats:italic>\n            is decreased both under basal conditions and in response\n to \u03b2adrenergic stimulation. Furthermore, flow-induced\n vasodilatation is impaired in isolated perfused carotid arteries, which\n express, like the heart, low levels of the protease. These data show\n that tissue kallikrein is the main kinin-generating enzyme\n            <jats:italic>in\n vivo<\/jats:italic>\n            and that a functional kallikrein\u2013kinin system is\n necessary for normal cardiac and arterial function in the mouse. They\n suggest that the kallikrein\u2013kinin system could be involved in the\n development or progression of cardiovascular diseases.\n          <\/jats:p>","DOI":"10.1073\/pnas.051619598","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T14:45:09Z","timestamp":1027694709000},"page":"2634-2639","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":146,"title":["Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice"],"prefix":"10.1073","volume":"98","author":[{"given":"Pierre","family":"Meneton","sequence":"first","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche\r M\u00e9dicale (INSERM) U367, 17 Rue du Fer \u00e0 Moulin, 75005\r Paris, France; Facult\u00e9 de M\u00e9decine\r Necker-Enfants Malades, Universit\u00e9 Paris V, 156 Rue de Vaugirard,\r 75015 Paris, France; Aventis, Disease Group\r Cardiovascular, Building H821, 65926 Frankfurt a.M., Germany;\r INSERM U541, 41 Boulevard de la Chapelle, 75010 Paris,\r France; Division of Hypertension, H\u00f4pital\r Universitaire, CH-1011 Lausanne, Switzerland; INSERM U400,\r Facult\u00e9 de M\u00e9decine, 8 Rue du..."}]},{"given":"May","family":"Bloch-Faure","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche\r M\u00e9dicale (INSERM) U367, 17 Rue du Fer \u00e0 Moulin, 75005\r Paris, France; Facult\u00e9 de M\u00e9decine\r Necker-Enfants Malades, Universit\u00e9 Paris V, 156 Rue de Vaugirard,\r 75015 Paris, France; Aventis, Disease Group\r Cardiovascular, Building H821, 65926 Frankfurt a.M., Germany;\r INSERM U541, 41 Boulevard de la Chapelle, 75010 Paris,\r France; Division of Hypertension, H\u00f4pital\r Universitaire, CH-1011 Lausanne, Switzerland; INSERM U400,\r Facult\u00e9 de M\u00e9decine, 8 Rue du..."}]},{"given":"Albert A.","family":"Hagege","sequence":"additional","affiliation":[{"name":"Institut National de 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