Cerebral blood flow during simulated central hypovolaemia in people with hypertension: does vertebral artery hypoplasia matter?

Adults with hypertension have higher prevalence of vertebral artery hypoplasia (VAH), which is associated with lower resting cerebral blood flow (CBF). We examined whether VAH impacts the ability to regulate CBF during haemodynamic stress when cardiac output and blood pressure are lowered via body negative pressure (LBNP). Participants underwent magnetic resonance angiography (MRA) at 1.5T during LBNP at 0, -20 and -40 mmHg, and were assigned to VAH (n = 13) or without-VAH (n = 11) groups post-acquisition. Phase-contrast MRA measured flow in the basilar artery (BA), internal carotid arteries (ICA), and the ascending aorta to measure cardiac output (CO). The CO decreased during all levels of LBNP in both groups (LBNP main effect P < 0.0001), whereas MAP was reduced in the group without VAH only (P = 0.0003). BA flow was reduced during LBNP in the group without VAH (P = 0.0267 at -20 mmHg and P < 0.0001 at -40 mmHg) but was surprisingly unchanged in the group with VAH (P > 0.05 all levels LBNP). ICA flow decreased during LBNP (P < 0.0001) and was not different between groups. Total CBF decreased during LBNP in hypertensives without VAH (P = 0.0192 at -20 mmHg and P < 0.0001 at -40 mmHg) but was unchanged in patients with VAH (P > 0.05 at all levels of LBNP). Total peripheral resistance (TPR) increased during LBNP in both groups, but the rise was greater in the group with VAH (-20 mmHg; P = 0.0129, -40 mmHg; P = 0.0016). In summary, hypertensive patients without VAH may tolerate decreases in CBF, whereas patients with VAH evoke a greater systemic TPR response to preserve CBF. KEY POINTS: Vertebral artery hypoplasia (VAH) is more common in hypertensive adults and is associated with lower resting cerebral blood flow (CBF), suggesting that VAH might impair the brain's ability to maintain cerebral blood flow during haemodynamic stress using lower body negative pressure. This study shows that hypertensive patients with VAH maintain CBF during body negative pressure, unlike those without VAH, who experience reductions in CBF. Patients with VAH show a greater rise in total peripheral resistance (TPR), suggesting a compensatory mechanism to maintain cerebral perfusion. The findings highlight that patients with VAH have an altered physiological response to hypovolaemia, where they may rely on systemic pressor responses to maintain perfusion of posterior brain territories in already hypoperfused circulation. This is important for understanding how VAH impacts cerebrovascular function in hypertensive patients and may influence clinical approaches to managing CBF in disease conditions.