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Updated: Aug 16, 2026
07:18
Evaluation of Capillary and Other Vessel Contribution to Macular Perfusion Density Measured with Optical Coherence Tomography Angiography
Published on: February 18, 2022
Disparity in osmolarity-induced vascular reactivity
El Rasheid Zakaria1, C Michelle Hunt, Na Li
1Department of Physiology and Biophysics, Health Sciences Center A-1115, University of Louisville, Louisville, KY 40292, USA. erzaka01@louisville.edu
Journal of the American Society of Nephrology : JASN
|August 5, 2005
Summary
Peritoneal dialysis solutions (PDS) contain vasoactive components, primarily hyperosmolality and lactate. Glucose in PDS causes vasodilation in small intestinal vessels via adenosine receptors.
Area of Science:
- Physiology
- Pharmacology
- Nephrology
Background:
- Conventional peritoneal dialysis solutions (PDS) are known to be vasoactive.
- Understanding the specific vasoactive components and their mechanisms is crucial for optimizing dialysis therapy.
Purpose of the Study:
- To identify and quantitatively describe the vasoactive components within PDS.
- To elucidate the mechanisms underlying PDS-induced vascular effects.
Main Methods:
- In vivo intravital microscopy of rat jejunal microvasculature.
- Ex vivo study of vascular reactivity in rat aortic rings (endothelium-intact and -denuded).
- Assessment of solutions containing glucose or mannitol, with varying osmolality and pH, and lactate-containing solutions.
Main Results:
- Hypertonic glucose and mannitol induced vascular reactivity and relaxation.
- Lactate in low-pH solution caused significant force generation in aortic rings.
- Isotonic glucose selectively caused time-dependent vasodilation in intestinal premucosal arterioles, mediated by adenosine receptors.
Conclusions:
- Hyperosmolality and lactate are the primary vasoactive components in PDS.
- Vessel size and solute metabolic activity influence PDS vasoactivity.
- Glucose-induced vasodilation in visceral microvasculature involves adenosine receptors and cellular energy-dependent transport.
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