Abstract:
Endothelial dysfunction is a hallmark of hypertension and other vascular diseases.
Endothelial nitric oxide synthase (eNOS) is essential for endothelial function and
homeostasis, and eNOS dysregulation is a key common pathophysiologic step in several
cardiovascular disease states. In this study, we examined the vascular function in response
to dietary phosphate, which has been reported to regulate hypertension. C57bL/6 male
mice were subcutaneously implanted with either saline or Ang II Infusion mini-osmot ic
pumps (0.25 uL/hour for 28 days) before the diet protocol and underwent the 2-week
control diet of 0.3% and 2-week phosphate diet (0.15%, 0.3%, 1.5%P). After that, the
mice were sacrificed, and flow cytometry for the analysis of immune cells was performed
on the aorta of control and Ang II-infused mice receiving the corresponding P-rich diet
(0.15%,0.3%,1.5%P).Vascular reactivity studies by Wire myography for thoracic aortas
were performed. To further assess vascular function, eNOS protein and superoxide are to
be measured in aorta samples. Our data showed that high phosphate diet (1.5% P) reduced
blood pressure following hypertensive stimuli. However, high phosphate diet exhibited a
deleterious effect on the endothelial function and vascular inflammation especially in the
hypertensive Ang II-infused mice. Thus, the role of phosphate in hypertension requires
additional studies to dissect the mechanisms involved in mediating its effect on the
vasculature.
