{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T19:07:13Z","timestamp":1789585633173,"version":"build-2803163510"},"reference-count":56,"publisher":"Wiley","issue":"23","license":[{"start":{"date-parts":[[2018,4,25]],"date-time":"2018-04-25T00:00:00Z","timestamp":1524614400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000975","name":"Kidney Health Australia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000975","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001782","name":"University of Melbourne","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001782","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001030","name":"National Heart Foundation of Australia","doi-asserted-by":"publisher","award":["100519"],"award-info":[{"award-number":["100519"]}],"id":[{"id":"10.13039\/501100001030","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["400003"],"award-info":[{"award-number":["400003"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["1089763"],"award-info":[{"award-number":["1089763"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\"><jats:list-item><jats:p>Low weight at birth increases the risk of developing chronic diseases in adulthood<\/jats:p><\/jats:list-item><jats:list-item><jats:p>A diet that is high in salt is known to elevate blood pressure, which is a major risk factor for cardiovascular and kidney diseases<\/jats:p><\/jats:list-item><jats:list-item><jats:p>The present study demonstrates that growth restricted male rats have a heightened sensitivity to high dietary salt, in the context of raised systolic blood pressure, reduced urinary sodium excretion and stiffer mesenteric resistance vessels<\/jats:p><\/jats:list-item><jats:list-item><jats:p>Other salt\u2010induced effects, such as kidney hyperfiltration, albuminuria and glomerular damage, were not exacerbated by being born small<\/jats:p><\/jats:list-item><jats:list-item><jats:p>The present study demonstrates that male offspring born small have an increased cardiovascular susceptibility to high dietary salt, such that that minimizing salt intake is probably of particular benefit to this at\u2010risk population<\/jats:p><\/jats:list-item><\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>Intrauterine growth restriction increases the risk of developing chronic diseases in adulthood. Lifestyle factors, such as poor dietary choices, may elevate this risk. We determined whether being born small increases the sensitivity to a dietary salt challenge, in the context of hypertension, kidney disease and arterial stiffness. Bilateral uterine vessel ligation or sham surgery (offspring termed Restricted and Control, respectively) was performed on 18\u2010day pregnant Wistar Kyoto rats. Male offspring were allocated to receive a diet high in salt (8% sodium chloride) or remain on standard rat chow (0.52% sodium chloride) from 20 to 26\u00a0weeks of age for 6\u00a0weeks. Systolic blood pressure (tail\u2010cuff), renal function (24\u00a0h urine excretions) and vascular stiffness (pressure myography) were assessed. Restricted males were born 15% lighter than Controls and remained smaller throughout the study. Salt\u2010induced hypertension was exacerbated in Restricted offspring, reaching a peak systolic pressure of \u223c175\u00a0mmHg earlier than normal weight counterparts. The natriuretic response to high dietary salt in Restricted animals was less than in Controls and may explain the early rise in arterial pressure. Growth restricted males allocated to a high salt diet also had increased passive arterial stiffness of mesenteric resistance arteries. Other aspects of renal function, including salt\u2010induced hyperfiltration, albuminuria and glomerular damage, were not exacerbated by uteroplacental insufficiency. The present study demonstrates that male offspring exposed to uteroplacental insufficiency and born small have an increased sensitivity to salt\u2010induced hypertension and arterial remodelling.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp275655","type":"journal-article","created":{"date-parts":[[2018,3,31]],"date-time":"2018-03-31T15:57:14Z","timestamp":1522511834000},"page":"5859-5872","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Uteroplacental insufficiency temporally exacerbates salt\u2010induced hypertension associated with a reduced natriuretic response in male rat offspring"],"prefix":"10.1113","volume":"596","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0471-8517","authenticated-orcid":false,"given":"Linda A.","family":"Gallo","sequence":"first","affiliation":[{"name":"Department of Physiology The University of Melbourne VIC Australia"},{"name":"School of Biomedical Sciences The University of 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