Abstract P015: Bilateral Common Carotid Artery Stenosis in Hypertensive Rats Impairs Dilation in Penetrating Arterioles and Posterior Communicating Arteries [Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception]

Hypertension and chronic cerebral hypoperfusion (CCH) are leading risk factors for cognitive impairment. We induced hypoperfusion in stroke prone spontaneously hypertensive rats (SHRSP) by bilateral carotid artery stenosis (BCAS) to create a novel, physiologically relevant model of cognitive impairment. We hypothesized that BCAS in SHRSP would impair endothelium dependent dilation and lead to outward remodeling of the penetrating arterioles (PAs) and posterior cerebral arteries (PCAs). The PAs are critical for maintaining parenchymal perfusion and controlling blood flow to the neurovascular unit, and the PCAs are integral in regulating the severity of CCH. Both artery types were studied by pressure myography and data are shown as mean±SEM, SHAM vs BCAS (an n=4 to 12 in each group) with p<0.05. Short-term memory, evaluated by novel object recognition testing, was impaired 8 weeks after BCAS (novel exploration quotient: 0.60±0.1 vs 0.45±0.1). Endothelium-dependent dilation was assessed with carbachol (data shown as % dilation at 10-6M). BCAS impaired endothelial function in PAs, as evidenced by the abolition of the dilation (14±3.3% vs -10±4.7%) but did not significantly alter sodium nitroprusside induced dilation (60 ± 9.7% vs. 49 ± 6.4%). Inhibition of nitric oxide and prostacyclin production with L-NAME (100 μM) and indomethacin (10 μM), respectively, did not change dilation in either group. This suggests that endothe...
Source: Hypertension - Category: Cardiology Authors: Tags: Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception Source Type: research