ArticleActa physiologica (Oxford, England)2026
Impaired Renal Base Excretion in Secretin Receptor Knock-Out Mice During Prolonged Base-Loading.
Article in Acta physiologica (Oxford, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimSecretin was recently found to play a pivotal role in the renal adaptation to acute base excess. Here, secretin increases pendrin-dependent HCO
methodsUrine and blood acid-base analyses were carried out in secretin receptor (SCTR) KO and WT mice at baseline and after 1 and up to 8 days of base-loading with NaHCO
resultsSCTR KO mice responded with diminished urine alkalization and a lesser reduction of urinary acid excretion when base-loaded for 48 h. Concordantly, SCTR KO mice presented with increased blood base retention compared with WTs. Base-loaded SCTR WT and KO mice showed comparable total pendrin protein abundance. Despite this, pendrin function was markedly lower in SCTR KO mice. Base-loaded mice had higher plasma secretin and renal SCTR levels compared with acid-loaded mice. Higher arterial HCO
conclusionLoss of the SCTR diminishes renal base excretion capacity and exacerbates systemic base accumulation during prolonged base-loading. Further, plasma secretin and renal SCTR mRNA levels are modulated by acid-base intake. These findings further support a central role of secretin and its receptor in the regulation of both acute and prolonged base excess.
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