Publications by authors named "Pauline I de Bruijn"
Hyperaldosteronism after decreased renal K+ excretion in KCNMB2 knockout mice.
Am J Physiol Renal Physiol
May 2016
The kidney is the primary organ ensuring K(+) homeostasis. K(+) is secreted into the urine in the distal tubule by two mechanisms: by the renal outer medullary K(+) channel (Kir1.1) and by the Ca(2+)-activated K(+) channel (KCa1.
View Article and Find Full Text PDFThe loop diuretic furosemide inhibits NaCl reabsorption in the thick ascending limb (TAL). In addition, furosemide acidifies the urine, which is traditionally explained by increased Na+ loading to the distal tubule causing an activation of H+ secretion via H+-ATPase in α-intercalated cells. The inability to acidify urine in response to furosemide serves to diagnose distal renal tubular acidosis (dysfunction of α-intercalated cells).
View Article and Find Full Text PDFArticle Synopsis
- Urinary tract infections often result from Escherichia coli producing α-hemolysin (HlyA), which can cause significant damage to red blood cells (erythrocytes) through the activation of P2X receptors by ATP release.
- HlyA also triggers calcium ion ([Ca(2+)]i) oscillations in renal epithelial cells, leading to the release of inflammatory cytokines like interleukin-6 (IL-6) and IL-8; this process appears to depend on ATP release and P2Y2 receptor activation.
- Experiments show that blocking ATP scavenging or lacking P2Y2 receptors prevents these [Ca(2+)]i oscillations and IL-6 release, highlighting ATP
Extracellular nucleotides regulate epithelial transport via luminal and basolateral P2 receptors. Renal epithelia express multiple P2 receptors, which mediate significant inhibition of solute absorption. Recently, we identified several P2 receptors in the medullary thick ascending limb (mTAL) including luminal and basolateral P2Y(2) receptors (Jensen ME, Odgaard E, Christensen MH, Praetorius HA, Leipziger J.
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