Hypertension, Vol 7, 196-203, Copyright © 1985 by American Heart Association
DH Streeten, JH Auchincloss Jr, GH Anderson Jr, RL Richardson, FD Thomas and JW Miller
Among 1800 referred hypertensive patients, 181 had recumbent diastolic
blood pressures (DBP) below 90 mm Hg and standing DBP above 90 mm Hg.
Orthostatic increments in DBP were greater in these orthostatic
hypertensive patients than in 181 persistently hypertensive patients and
134 normotensive subjects. In 12 patients with orthostatic hypertension,
the orthostatic fall in cardiac output (27.3 +/- 2.9%, measured by a
respiratory method) was double that in 8 normotensive subjects (13.3 +/-
3.7%, p less than 0.01). An inflated pressure suit over the pelvis and
lower limbs prevented the excessive fall in cardiac output and
significantly reduced (p less than 0.02) the excessive rise in standing DBP
in orthostatic hypertensive patients. Gravitational pooling of blood in the
legs and reduction of blood in the head was measured by external gamma
counting of autologous erythrocytes labeled with sodium pertechnetate Tc
99m through ports in fixed positions over the leg and the temple.
Orthostatic intravascular pooling was significantly greater (p less than
0.01) in orthostatic hypertensive subjects than in normotensive subjects,
and the magnitudes of orthostatic pooling and orthostatic increases in DBP
were closely correlated (r = +0.85). Plasma norepinephrine concentrations
were similar in recumbency and after sustained handgrip exercise, but
significantly greater (p less than 0.01) after 5 to 60 mins of standing in
orthostatic hypertensive subjects than in normotensive subjects. Our
results indicate that orthostatic hypertension is common and that its
mechanism in representative patients involves excessive orthostatic blood
pooling, which results in decreased venous return, decreased cardiac
output, increased sympathetic stimulation (presumably through low-pressure
cardiopulmonary receptors), and excessive arteriolar, but not venular,
constriction.
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Orthostatic hypertension. Pathogenetic studies
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