Over 80% of ischemic stroke patients show an abrupt increase in blood pressure (BP) in the hours and days following stroke; yet whether post-stroke hypertension is beneficial or harmful remains controversial, and the underlying physiological basis is unclear. To investigate the dynamic cardiovascular response to stroke Wistar rats (n=6, 393±34g) were placed under isofluorane anesthesia (~3%), and instrumented with radio telemeters to record BP, ICP and brain tissue oxygen (P02) in the stroke penumbra. After a 1-week recovery period, an ischemic stroke was induced via middle cerebral artery occlusion on Day 0; recordings continued for 10 further days. Immediately following stroke, penumbra P02 decreased to less than half baseline levels during occlusion, but increased back to baseline levels with reperfusion. BP increased rapidly from baseline (108±9mmHg) to a peak of +44±7mmHg above baseline, before recovering by Day 10 (+4±3mmHg). In contrast, ICP increased more gradually from baseline (5±1mmHg), to a peak of +25±8mmHg on Day 3, and recovering to +4±2mmHg above baseline at Day 10. This is consistent with the formation of cerebral oedema. Calculated as the difference between BP and ICP, cerebral perfusion pressure (CPP) increased 24-48 hours after stroke (+27±11mmHg) and decreased by -13±7mmHg during Days 3-4, subsequently returning to baseline. These findings suggest that the increase in BP immediately after ischemic stroke is temporally matched to the fall in brain tissue P02. However, the observed delayed rise in ICP does not elicit a matched increase in BP, thus CPP falls, before recovering to baseline. These results indicate that cerebral ischemia may be the primary initial trigger for post-stroke hypertension.