Abstract
Preeclampsia (PE), a dangerous hypertensive complication of pregnancy, is associated with widespread maternal vascular dysfunction. However, the effect of PE on the cerebral vasculature that can lead to stroke and cognitive decline is not well understood. We hypothesized that function of cortical parenchymal arterioles (PAs) would be impaired during PE. Using a high cholesterol diet to induce experimental PE in rats (ePE), we studied the function and structure of isolated and pressurized PAs supplying frontoparietal white matter (WM) tracts and cortex and compared to normal pregnant (Preg) and nonpregnant (Nonpreg) Sprague Dawley rats (n = 8/group). Myogenic reactivity and tone were similar between groups; however, constriction to intermediate-conductance calcium-activated potassium (IK) channel inhibition was diminished and dilation to inward-rectifying K+ (KIR) channel activation was impaired in PAs from ePE rats, suggesting altered ion channel function. Conducted vasodilation was significantly delayed in response to 12 mM KCl, but not 10 μM adenosine, in PAs from ePE rats versus Preg and Nonpreg rats (940 ± 300 ms vs. 70 ± 50 ms and 370 ± 90 ms; p < 0.05). Overall, dysfunction of PAs supplying frontoparietal WM and gray matter was present in ePE. If persistent these changes could potentiate neuronal injury that over time could contribute to WM lesions and early-onset cognitive decline.
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