The impact of ropinirole on blood pressure and noradrenaline concentration after active orthostasis in Parkinsonian patients.

Orthostatic hypotension is common in Parkinsonian patients. It is probably caused by reduced noradrenaline (NA) release. This effect is further enhanced by therapeutic use of ergot alkaloid dopamine agonists. In this trial we studied the impact of the non-ergot dopamine agonist ropinirole on blood pressure and noradrenaline release in 12 patients suffering from idiopathic parkinsonism (six female, six male, mean age 57.6+/-4.9years). Only de novo patients were included in this study. These patients were started on ropinirole monotherapy. In all patients blood pressure and serum noradrenaline levels at rest were measured supine (after lying down for 10min) and standing (9th minute after positional change). Patients with a drop in blood pressure >10mmHg were excluded from the study. Measurements were repeated after treatment with ropinirole 6mg/day. Before treatment the NA concentration (determined via HPLC) went up by 390.1pg/ml (SD 54) to the 9th minute after rising, but during management with ropinirole it went up only by 338.4+/-78pg/ml. In controls (n=27; eight women, 19 men, aged 60.6+/-10.8years) NA increased by 425+/-230pg/ml. The NA increase thus differed substantially prior to therapy compared with controls, and the difference did not change significantly during treatment. With ropinirole eight patients showed normal, four patients borderline and none of them pathologic decrease in blood pressure. These results do show a small but nonsignificant influence of the non-ergot dopamine agonist on blood pressure response and noradrenaline release, which is much less prominent than the change observed with ergot dopamine agonists.