Orthostatic hypertension. Pathogenetic studies.

Abstract

SUMMARY 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 < 0.01). An inflated pressure suit over the pelvis and lower limbs prevented the excessive fall in cardiac output and significantly reduced (p < 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 < 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 < 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. (Hypertension

Exaggerated Postural Blood Pressure Rise Is Related to a Favorable Outcome in Patients With Acute Ischemic Stroke

“…Spontaneous reduction of BP after vessel recanalization also implies stroke-specific mechanisms. 25 Several underlying mechanisms like damage to cardiovascular and autonomic brain centers, 26 an excessive reaction to venous pooling in the legs, 27 an increased sympathetic nervous system and/or reduced parasympathetic activity, an impaired cardiac baroreceptor sensitivity, and raised levels of circulating catecholamines may all contribute to this hypertensive response. 28,29 Our results relate favorable outcome to an exaggerated postural BP increase without important contributions of HR.…”

Severely Impaired Baroreflex-Buffering in Patients With Monogenic Hypertension and Neurovascular Contact

“…Similarly, leg compression prevents the orthostatic increase in blood pressure in patients with orthostatic hypertension. 21 Moreover, stimuli such as cold pressor testing and hand-grip exercise led to a greater than normal pressor response. Although blood pressure responses to these stimuli were excessive, the increase in muscle sympathetic nerve activity was moderate.…”

Population-Based Study on the Prevalence and Correlates of Orthostatic Hypotension/Hypertension and Orthostatic Dizziness

“…Our data adopted the same criterion as the previous study and revealed that the prevalence of OHT was 1.1% in study subjects aged 20-84 years and 4.6% in elderly subjects. Although the mechanism of OHT is not well understood, it maybe involve excessive orthostatic venous pooling, which leads to decreased cardiac output, augmented sympathetic stimulation, and finally excessive arteriolar constriction (31). Further study is needed to determine whether or not the discrepancy in the prevalence of OHT is related to the difference in autonomic function due to ethnic effect.…”