Vasomotor conduction is not augmented in hypertensive stroke‐prone rats following middle cerebral artery occlusion.

Spontaneously hypertensive stroke‐prone rats (SHRSP) exhibit markedly greater infarct after middle cerebral artery occlusion (MCAO) as compared to normotensive rats. The difference in stroke damage may be related to anatomical or functional differences in the cerebral collateral vasculature. We have previously demonstrated that ischemia‐reperfusion (I/R) augmented vasomotor conduction in cerebral arterioles. In the present study, we tested the hypothesis that augmentation of conducted vasodilation is lacking in SHRSP after I/R. MCAO (2 h occlusion and 24 h reperfusion) was performed in SHRSP with an intraluminal filament method. Penetrating arteriolar branches of the MCA were isolated and cannulated with a concentric micropipette system. Both ischemic (n=4) and sham‐control (n=7) arterioles developed similar myogenic tone (~70% of passive diameter, 60 mmHg). Local micropipette‐application of ATP onto these arterioles evoked a biphasic constriction (15 ± 3%) and dilation (8±3%) response. These local responses spread longitudinally along both sham and ischemic arterioles (1 mm conduction distance), but with rapid spatial decay. Thus, conducted vasomotor responses in SHRSP arterioles were not enhanced after I/R. We speculate that the lack of augmentation of vasomotor conductivity may contribute to increased tissue injury in SHRSP following MCAO.