[Stimulation of the central dopaminergic receptor in essential hypertensive patients using amantadine]

At present, evidence has been accumulating that point out that some central nervous structures, of oblongata to the limbic system, are primarily involved in the control of systemic arterial pressure (AP). In agreement with several experimental and clinical works, a hypothesis has been suggested that a functional defect of the central dopaminergic system could be involved in the etiopathogenesis of essential hypertension (EH). With the objective of analyzing this hypothesis, the effect of dopamine (DA) agonist, amantadine (Am) on heart rate (HR), AP, plasma catecholamines (CA, PCA), urinary DA, noradrenaline (NA), adrenaline (A), vanilmandelic acid (VMA) and homovanillic acid (HVA), was studied in 19 females with established EH. The study included 2 periods: "placebo" and "drug", each one lasting 22 days, with a register of HR and AP in clino and orthostatism, taken every 3-4 days; at the end of each period, CA and their metabolites were measured. During the drug period, oral Am clorhidrate (300 mg/day, t.i.d.) was administered. With the drug, HR was not change with respect to the placebo period; but the AP in both positions, just as PCA, DA, NA and HVA, showed a highly significant decrease; A and VMA displayed a less significant decrease from the statistical point of view. The obtained results and literature data support the hypothesis that in EH there probably exists a genetic disfunction of the inhibitory central dopaminergic receptor of peripheral sympathetic activity, which is susceptible to compensation by use of several dopaminergic agonists, such as Am.