Neurohormonal behavior during prolonged orthostatic stress in normotensive subjects

Prolonged orthostatic stress induces major changes in hemodynamic and autonomic nervous system function. The neurohormonal response to acute and prolonged orthostatic stress that may trigger neurocardiogenic syncope is not clear. The goal of this study was to assess neurohormonal changes during acute and prolonged orthostatic stress. In fifteen normotensive subjects without medication blood was sampled at supine rest (S), during early passive orthostatic stress (after first 10 min.) (T1) and after prolonged (>40 min.) orthostatic stress (T2). We measured atrial and brain natriuretic peptides (ANP and BNP) and catecholamines [norepinephrine (NOR), epinephrine (EPI) and dopamine (DOP)]. ANP was 7.0 +/- 4.3 pmol/l during S, 7.3 +/- 5.1 during T1 and 4.6 +/- 2.8 during T2 (NS and p < 0.05). BNP was 1.9 +/- 1.6 pmol/l during S, 1.7 +/- 1.5 during T1 and 1.4 +/- 1.3 during T2 (p < 0.05 and p < 0.05). NOR was 172 +/- 92 pg/ml during S, 378 +/-_216 during T1 and 402 +/- 183 during T2 (p < 0.01 and NS). EPI was 10.4 +/- 3.8 pg/ml during S, 22.2 +/- 9.3 during T1 and 44.4 +/- 26.0 during T2 (p < 0.01 and p < 0.01). DOP was 7.8 +/- 4.8 pg/ml, 7.6 +/- 2.1 during T1 and 7.0 +/- 2.3 during T2 (NS and NS), Neurohormonal responses to orthostatic stress varied. Natriuretic peptides (ANP and BNP) decreased with prolonged orthostatic stress, probably due to the progressive hypovolemia it induced. Dopamine levels did not change, whereas norepinephrine and epinephrine showed a considerable rise following acute orthostatic stress, with epinephrine rising still further with prolonged orthostatic stress. Neurohormonal responses to prolonged orthostatic stress could help to clarify the pathophysiology of neurocardiogenic syncope.