English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Dysregulation of the expression/shuttling of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in renal collecting duct principal cells has been found in animal models of hypertension. We tested whether a similar dysregulation exists in essential hypertension.    Methods  We measured urinary excretion of AQP2 and ENaC β-subunit corrected for creatinine (u-AQP2 CR , u-ENaC β-CR ), prostaglandin E2 (u-PGE 2 ) and cyclic AMP (u-cAMP), fractional sodium excretion (FE Na ), free water clearance (C H2O ), as well as plasma concentrations of vasopressin (AVP), renin (PRC), angiotensin II (Ang II), aldosterone (Aldo), and atrial and brain natriuretic peptide (ANP, BNP) in 21 patients with essential hypertension and 20 normotensive controls during 24-h urine collection (baseline), and after hypertonic saline infusion on a 4-day high sodium (HS) diet (300 mmol sodium/day) and a 4-day low sodium (LS) diet (30 mmol sodium/day).    Results  At baseline, no differences in u-AQP2 CR  or u-ENaC β-CR  were measured between patients and controls. U-AQP2 CR  increased significantly more after saline in patients than controls, whereas u-ENaC β-CR  increased similarly. The saline caused exaggerated natriuretic increases in patients during HS intake. Neither baseline levels of u-PGE 2 , u-cAMP, AVP, PRC, Ang II, Aldo, ANP, and BNP nor changes after saline could explain the abnormal u-AQP2 CR  response.    Conclusions  No differences were found in u-AQP2 CR  and u-ENaC β-CR  between patients and controls at baseline. However, in response to saline, u-AQP2 CR  was abnormally increased in patients, whereas the u-ENaC β-CR  response was normal. The mechanism behind the abnormal AQP2 regulation is not clarified, but it does not seem to be AVP-dependent.    Clinicaltrial.gov identifier   NCT00345124 .

Abnormal increase in urinary aquaporin-2 excretion in response to hypertonic saline in essential hypertension