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SUMMARY Bromocriptine (Br) was used to test the hypothesis that central dopaminergic mechanisms modulate sympathetic nerve tone, and that when dopaminergic control is deficient there may result enhanced noradrenergic activity and elevated blood pressure (BP) in some patients with primary hypertension. Seven hypertensive patients (age 29 ± 3 years) were studied after a single oral dose of Br (2.5-5.0 mg) and after 1 week of treatment with Br (5-15 mg/day). The data were compared to those obtained during respective placebo periods. The Br reduced systolic blood pressure (SBP) and diastolic blood pressure (DBP) during supine, sitting, and standing positions and mild mental stress but not during isometric handgrip exercise. Orthostatic hypotension occurred in all patients after the first dose of Br but was present only In one patient after 1 week of treatment. Pretreatment levels of plasma norepinephrine (NE) in supine and standing positions were elevated as compared to previously obtained data of normal controls. After 1 week of Br therapy, plasma NE was reduced 40% to 50% in supine, sitting, and standing positions, and during isometric handgrip exercise (p < 0.05). Plasma NE after a single dose of Br was not different from that found after 1 week of the drug. Excretion rates of urinary NE and normetanephrine (NM) were lower (p < 0.002 and p < 0.005 respectively) during Br as compared to pretreatment values. Sodium excretion tended to be higher and plasma renin activity (PRA) lower after 1 week of Br, but the differences were not significant. Dopaminergic stimulation by Br, probably central in location, reduces sympathetic outflow and thereby might contribute to lowering of BP in primary hypertension. These findings support the hypothesis that reduced central dopaminergic activity may be a factor in the cause and maintenance of primary hypertension.

Dopaminergic control of sympathetic tone and blood pressure: evidence in primary hypertension.