Sympathoexcitatory responses to the acute blood pressure fall induced by central or peripheral antihypertensive drugs

This study was designed to evaluate the effects of an acute blood pressure reduction brought about by a peripheral vasodilator agent (prazosin) or by a drug combining central and peripheral modes of action (urapidil), on thre e markers of adrenergic tone such as muscle sympathetic nerve traffic (MSNA ), venous plasma norepinephrine (NE), and heart rate (HR). In 12 untreated essential hypertensives (age, 50.7 +/- 1.9 years; mean +/- SEM), we evaluat ed in two experimental sessions, according to a double-blind crossover desi gn, the effects of acute oral administration of 2 mg prazosin or 30 mg urap idil on beat-to-beat finger blood pressure (Finapres), HR (electrocardiogra m), NE (high-performance liquid chromatography), and MSNA (microneurography at a peroneal nerve). In each session measurements were performed in the n o-drug control state and repeated throughout a 3-h period after drug admini stration. For similar blood pressure reductions, the two drugs caused simil ar increases in NE and MSNA (peak effects: NE = +1.1 +/- 0.2 vs 0.9 +/- 0.2 nmol/L and MSNA +10.9 +/- 1.8 vs +10.1 +/- 1.6 bursts/min for prazosin and urapidil respectively, P = ns between drugs), whereas HR increased more ma rkedly after prazosin administration (+6.1 +/- 1.1 vs +2.4 +/- 0.8 beats/mi n, P < 0.05). These data provide evidence that acute blood pressure reducti ons induced by antihypertensive drugs with central or peripheral modes of a ction activate the sympathetic nervous system to a similar extent. Thus adr energic activation is not peculiar to vasodilators but rather generalized t o any drug-induced acute blood pressure fall, presumably because of the lac k of a baroreflex resetting, which occurs during chronic but not during acu te antihypertensive treatment. (C) 2000 American Journal of Hypertension, L td.