{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T01:18:59Z","timestamp":1791249539972,"version":"4.1.0"},"reference-count":13,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1999,8]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Kinins have been implicated in the hemodynamic adaptation to postnatal life. The present study examined the impact of bradykinin B\n            <jats:sub>2<\/jats:sub>\n            receptor (B\n            <jats:sub>2<\/jats:sub>\n            R) gene disruption on the postnatal changes in blood pressure (BP) and the susceptibility to early onset salt-sensitive hypertension in mice. B\n            <jats:sub>2<\/jats:sub>\n            R null (\u2212\/\u2212) and wild-type (+\/+) mice were fed normal (NS, 1% NaCl) or high (HS, 5% NaCl) salt diets during pregnancy. After birth, the pups remained with their mothers until they were weaned and were subsequently continued on the respective maternal salt intake until 4 months of age. The age-related changes at 3 and 4 months in tail-cuff BP and anesthetized mean arterial pressure at 4 months were not different in NS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            and NS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>+\/+<\/jats:sup>\n            mice. However, there was a mild increase in BP in NS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            at 2 months versus NS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>+\/+<\/jats:sup>\n            . In contrast, HS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice manifested early onset and persistent elevations of tail-cuff BP (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) at 2, 3, and 4 months versus other groups. MAP was also higher in HS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            than HS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>+\/+<\/jats:sup>\n            , NS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            , and NS\/B\n            <jats:sub>2<\/jats:sub>\n            R\n            <jats:sup>+\/+<\/jats:sup>\n            (91\u00b13 versus 75\u00b15, 74\u00b12, and 70\u00b12 mm Hg, respectively;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Kidney renin and angiotensin type 1 receptor mRNA levels were not different. Additional studies showed that a delay in the initiation of HS until after birth was accompanied by later development of hypertension, although postnatal discontinuation of HS resulted in a gradual return of BP to normal values by 4 months of age. The results demonstrate that (1) kinins protect the developing animal from salt-sensitive hypertension, (2) lack of B\n            <jats:sub>2<\/jats:sub>\n            R from early development does not alter the maturation of BP under conditions of normal sodium intake, and (3) exposure to a HS diet during fetal life is not sufficient in itself to induce long-term hypertension in either wild-type or B\n            <jats:sub>2<\/jats:sub>\n            R null mice.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.34.2.176","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"176-180","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":62,"title":["Early Onset Salt-Sensitive Hypertension in Bradykinin B\n            <sub>2<\/sub>\n            Receptor Null Mice"],"prefix":"10.1161","volume":"34","author":[{"given":"Ludek","family":"Cervenka","sequence":"first","affiliation":[{"name":"From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M.","family":"Harrison-Bernard","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susana","family":"Dipp","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ginny","family":"Primrose","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John D.","family":"Imig","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samir S.","family":"El-Dahr","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.13706"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.29.1.483"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.96.10.3570"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.31.6.1278"},{"key":"e_1_3_2_5_2","first-page":"F705","volume":"262","year":"1992","unstructured":"El-Dahr SS, Chao J. 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