Cerebral vasomotor reactivity before and after blood pressure reduction in hypertensive patients

Hypertension is associated with cerebrovascular remodeling and endothelial dysfunction, which may reduce cerebral vasomotor reactivity to CO2. Treatment combining blood pressure (BP) reduction with inhibition of vascular effects of angiotensin II may reverse these changes. However, the reduction in BP at the onset of treatment can compromise cerebral perfusion and exhaust vasomotor reserve, leading to impaired CO2 reactivity.

Eleven patients (nine men, two women) with newly diagnosed, untreated mild-to-moderate hypertension aged (mean (s.d.)) 52 (9) years, and eight controls (seven men, one woman) aged 46 (10) years were studied. Patients received losartan/hydrochlorothiazide (50/12.5 or 100/25 mg) to reduce BP to <140/<90 mm Hg within 1-2 weeks. BP (Finapres), heart rate (HR), CBFV (cerebral blood flow velocity, transcranial Doppler), cerebrovascular resistance, and CO2 reactivity were measured at baseline, after the rapid BP reduction, and after long-term treatment (3-4 months).

At baseline, hypertension was not associated with reduced CO2 reactivity. Treatment effectively lowered BP from 148 (12)/89 (7) to 130 (15)/80 (9) after 1-2 weeks and 125 (10)/77 (7) mm Hg after 3-4 months (P = 0.003). CO2 reactivity was not affected by the reduction in BP within 2 weeks, and long-term treatment did not augment reactivity.

In hypertension without diabetes or advanced cerebrovascular disease, CO2 reactivity is not reduced, and rapid normalization (within 2 weeks) of BP does not exhaust vasomotor reserve. CO2 reactivity did not change between 2 and 12 weeks of treatment, which argues against a direct vascular effect of angiotensin II inhibition within this period.