{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T06:40:38Z","timestamp":1790404838293,"version":"4.1.0"},"reference-count":51,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2023,1,15]],"date-time":"2023-01-15T00:00:00Z","timestamp":1673740800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000291","name":"Kidney Research UK","doi-asserted-by":"publisher","award":["RP\u2010023\u201020190306"],"award-info":[{"award-number":["RP\u2010023\u201020190306"]}],"id":[{"id":"10.13039\/501100000291","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000361","name":"Diabetes UK","doi-asserted-by":"publisher","award":["17\/0005685"],"award-info":[{"award-number":["17\/0005685"]}],"id":[{"id":"10.13039\/501100000361","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Type 1 diabetes mellitus (T1DM) leads to serious complications including premature cardiovascular and kidney disease. Hypertension contributes importantly to these adverse outcomes. The renal pressure natriuresis (PN) response, a key regulator of blood pressure (BP), is impaired in rats with T1DM as tubular sodium reabsorption fails to down\u2010regulate with increasing BP. We hypothesised that sodium\u2013glucose cotransporter 2 (SGLT2) inhibitors, which reduce cardiovascular risk in kidney disease, would augment the PN response in T1DM rats. Non\u2010diabetic or T1DM (35\u201350\u00a0mg\/kg streptozotocin <jats:sc>i.p.<\/jats:sc>) adult male Sprague\u2013Dawley rats were anaesthetised (thiopental 50\u00a0mg\/kg <jats:sc>i.p.<\/jats:sc>) and randomised to receive either dapagliflozin (1\u00a0mg\/kg <jats:sc>i.v.<\/jats:sc>) or vehicle. Baseline sodium excretion was measured and then BP was increased by sequential arterial ligations to induce the PN response. In non\u2010diabetic animals, the natriuretic and diuretic responses to increasing BP were not augmented by dapagliflozin. Dapagliflozin induced glycosuria, but this was not influenced by BP. In T1DM rats the PN response was impaired. Dapagliflozin again increased urinary glucose excretion but did not enhance PN. Inhibition of SGLT2 does not enhance the PN response in rats, either with or without T1DM. SGLT2 makes only a minor contribution to tubular sodium reabsorption and does not contribute to the impaired PN response in T1DM.<\/jats:p>","DOI":"10.1113\/ep090849","type":"journal-article","created":{"date-parts":[[2023,1,16]],"date-time":"2023-01-16T07:55:46Z","timestamp":1673855746000},"page":"480-490","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Sodium\u2013glucose cotransporter 2 inhibition does not improve the acute pressure natriuresis response in rats with type 1 diabetes"],"prefix":"10.1113","volume":"108","author":[{"given":"Natalie K.","family":"Jones","sequence":"first","affiliation":[{"name":"British Heart Foundation Centre for Cardiovascular Science University of Edinburgh  Edinburgh UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah M.","family":"Costello","sequence":"additional","affiliation":[{"name":"British Heart Foundation Centre for Cardiovascular Science University 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