{Reference Type}: Journal Article
{Title}: Cardiopulmonary deconditioning and plasma volume loss are not sufficient to provoke orthostatic hypertension.
{Author}: Hoenemann JN;Moestl S;de Boni L;Hoffmann F;Arz M;Berger L;Pesta D;Heusser K;Mulder E;Lee SMC;Macias BR;Tank J;Jordan J;
{Journal}: Hypertens Res
{Volume}: 47
{Issue}: 8
{Year}: 2024 Aug 23
{Factor}: 5.528
{DOI}: 10.1038/s41440-024-01710-x
{Abstract}: Orthostatic hypertension, defined by an increase of systolic blood pressure (SBP) of ≥20 mmHg upon standing, harbors an increased cardiovascular risk. We pooled data from two rigorously conducted head-down tilt bedrest studies to test the hypothesis that cardiopulmonary deconditioning and hypovolemia predispose to orthostatic hypertension. With bedrest, peak VO2 decreased by 6 ± 4 mlO2/min/kg (p < 0.0001) and plasma volume by 367 ± 348 ml (p < 0.0001). Supine SBP increased from 127 ± 9 mmHg before to 133 ± 10 mmHg after bedrest (p < 0.0001). In participants with stable hemodynamics following head-up tilt, the incidence of orthostatic hypertension was 2 out of 67 participants before bedrest and 2 out of 57 after bedrest. We conclude that in most healthy persons, cardiovascular deconditioning and volume loss associated with long-term bedrest are not sufficient to cause orthostatic hypertension.