Endothelium-dependent relaxation was significantly reduced in MWF rats compared to LEW or FHH rats (p < 0.05), indicating that proteinuria alone is insufficient to cause endothelial dysfunction.
Proteinuria alone does not universally cause endothelial dysfunction, indicating that additional strain-specific deleterious factors are required for vascular damage in renal disease.
p-value: p=<0.05
BACKGROUND: Proteinuria-associated endothelial dysfunction (ED) is assumed to play a main role in the cardiovascular morbidity in proteinuric patients. However, the connection between proteinuria and systemic endothelial function is not clear yet. Therefore, we studied aortic endothelial function in Munich Wistar Fromter (MWF) and fawn-hooded hypertensive (FHH) inbred rat strains with genetic proteinuria to determine the specific impact of proteinuria on the development of ED. METHODS: Proteinuria, cardiac function, systemic blood pressure, plasma lipid profiles, aortic endothelial function, plasma levels of cyclo-oxygenase products and dimethylarginines were investigated in 26-week-old inbred rat strains with (MWF and FHH) and without Lewis (LEW) rats proteinuric renal disease. RESULTS: The endothelium-dependent relaxation was significantly reduced in MWF (p < 0.05 vs. LEW or FHH). The plasma thromboxane B(2), prostaglandin F(2alpha) and prostaglandin E(2)levels were higher in MWF (p < 0.05 vs. LEW or FHH), whereas the 6-keto-prostaglandin F(1alpha) level was comparable in all groups. The arginine/asymmetric dimethylarginine ratio was highest in MWF. CONCLUSIONS: This study differentiates common risk factors for ED in renal disease. Despite clear-cut proteinuria, FHH rats were devoid of changes in aortic endothelial function, indicating that some other deleterious factors must accompany proteinuria in order for ED to ensue. Further exploration of this model may serve to dissect mechanistical pathways and guide the development of protective strategies in the vascular damage of renal disease.
Ulu et al. (Thu,) conducted a other in Proteinuria-associated endothelial dysfunction. Genetic proteinuria (MWF and FHH strains) vs. Lewis (LEW) rats without proteinuric renal disease was evaluated on Aortic endothelial function (endothelium-dependent relaxation) (p=<0.05). Endothelium-dependent relaxation was significantly reduced in MWF rats compared to LEW or FHH rats (p < 0.05), indicating that proteinuria alone is insufficient to cause endothelial dysfunction.
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