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AuthorZakaria, El Rasheid
AuthorAl-Thani, Asma
AuthorFawzi, Ashraf
AuthorFituri, Omar
Available date2016-01-12T12:00:11Z
Publication Date2014
Publication NameAdvances in Peritoneal Dialysisen_US
CitationZakaria el R, Althani A, Fawzi AA, Fituri OM, Hyperosmolality-mediated peritoneal microvascular vasodilation is linked to aquaporin function. Advances in Peritoneal Dialysis, 2014, 30:63-74
ISSN1197-8554
URIhttp://hdl.handle.net/10576/4073
AbstractGlucose-based peritoneal dialysis (PD) solutions dilate the parietal and visceral peritoneal microvasculature by endothelium-dependent mechanisms that primarily involve hyperosmolality. This PD-mediated dilation occurs by active intracellular glucose uptake and adenosine A1 receptor activation, and by hyperosmolality-stimulated glibenclamide-sensitive potassium channels. Both pathways invoke NO as a second messenger for vasodilation. We hypothesized that during crystalloid-induced osmosis, the osmotic water flux through the transendothelial water-exclusive aquaporin 1 (AQP1) channels is the primary mechanism whereby the endothelium is being stimulated to instigate hyperosmolality-driven vasodilation. Four microvascular levels (diameters in the range 6 – 100 μm) were visualized by intravital videomicroscopy of the terminal ileum in anesthetized rats. Microvascular diameters and flow were measured after topical exposure to a 5% hypertonic mannitol or 2.5% glucose-based PD solution, at baseline and after brief tissue pre-treatment (with 0.1% glutaraldehyde for 10 seconds) or after combined tissue pre-treatment and pharmacologic blockade of AQP1 with HgCl2 (100 μmol/L). Vascular endothelial integrity was verified by the response to acetylcholine (10–4 mol/L) and sodium nitroprusside (10–4 mol/L). The hyperosmolar solutions both caused rapid and sustained vasodilation at all microvascular levels, which was not altered by tissue pre-treatment. Inhibition of AQP1 completely abolished the mannitolinduced vasodilation and markedly attenuated the PD fluid–mediated vasodilation. Neither glutaraldehyde pre-treatment nor HgCl2 affected tissue integrity or endothelial cell function. We conclude that the peritoneal microvascular vasodilation caused by hyperosmolar PD fluid is instigated by the osmotic water flux through AQP1. Clinical PD solutions have components other than hyperosmolality that can induce endothelium-dependent peritoneal microvascular vasodilation independent of the AQP1-mediated osmosis.
Sponsorresearch grant NPRP 09-268-3-066, funded by the Qatar National Research Fund
Languageen
PublisherPeritoneal dialysis publications Inc
SubjectHyperosmolality
Subjectvascular reactivity
Subjectadenosine receptors
Subjectintestinal microcirculation
Subjectvasodilation
SubjectPeritoneal dialysis solution
SubjectGlucose/pharmacokinetics
SubjectIleum/metabolism
TitleHyperosmolality-Mediated Peritoneal Microvascular Vasodilation Is Linked to Aquaporin Function
TypeArticle
Pagination63-74
Volume Number30


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