Plasticity of cerebral microvascular structure and mechanics during hypertension and following recovery of arterial pressure

Changes in vascular structure contribute to vascular events and loss of brain health. We examined changes in cerebral arterioles at the onset of hypertension and the hypothesis that alterations during hypertension would recover with the return of mean arterial pressure (MAP) to normal. MAP was measured with radiotelemetry in awake male C57BL/6J mice at baseline and during infusion of vehicle or angiotensin II (ANG II, 1.4 mg/kg/day using osmotic pumps) for 28 days, followed by a 28-day recovery. With ANG II treatment, MAP increased through day 28. On day 30, MAP began to recover, reaching levels not different from vehicle on day 37. We measured intravascular pressure, diameter, wall thickness (WT), wall:lumen ratio (W:L), cross-sectional area (CSA), and slope of the tangential elastic modulus (ET) in maximally dilated arterioles. Variables were similar in both groups at day 1, with no significant change with vehicle treatment. With ANG II treatment, CSA, WT, and W:L increased on days 7-28. Internal and external diameter was reduced at 14 and 28 days. ET versus wall stress was reduced on days 7-28. During recovery, the diameter remained at days 14 and 28 values, whereas other variables returned partly or completely to normal. Thus, CSA, WT, W:L, and ET versus wall stress changed rapidly during hypertension and recovered with MAP. In contrast, inward remodeling developed slowly and did not recover. This lack of recovery has mechanistic implications for the long-term impact of hypertension on vascular determinants of brain health.NEW & NOTEWORTHY Changes in vascular structure contribute to vascular events and loss of brain health. We examined the inherent structural plasticity of cerebral arterioles during and after a period of hypertension. Arteriolar wall thickness, diameter, wall-to-lumen ratio, and biological stiffness changed rapidly during hypertension and recovered with blood pressure. In contrast, inward remodeling developed slowly and did not recover. This lack of recovery of arteriolar diameter has implications for the long-term impact of hypertension on vascular determinants of brain health.