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Eide I, Campese V, Stein D, et al. Clinical assessment of sympathetic tone: orthostatic blood pressure responses in borderline primary hypertension. Clin Exp Hypertens. 1978;1(1):51-65doi: 10.3109/10641967809068595.
Eide, I., Campese, V., Stein, D., Eide, K., & DeQuattro, V. (1978). Clinical assessment of sympathetic tone: orthostatic blood pressure responses in borderline primary hypertension. Clinical and experimental hypertension, 1(1), 51-65. https://doi.org/10.3109/10641967809068595
Eide, I, et al. "Clinical assessment of sympathetic tone: orthostatic blood pressure responses in borderline primary hypertension." Clinical and experimental hypertension vol. 1,1 (1978): 51-65. doi: https://doi.org/10.3109/10641967809068595
Eide I, Campese V, Stein D, Eide K, DeQuattro V. Clinical assessment of sympathetic tone: orthostatic blood pressure responses in borderline primary hypertension. Clin Exp Hypertens. 1978;1(1):51-65. doi: 10.3109/10641967809068595. PMID: 755646.
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Clin Exp Hypertens. 1978;1(1):51-65. doi: 10.3109/10641967809068595.

Clinical assessment of sympathetic tone: orthostatic blood pressure responses in borderline primary hypertension.

Clinical and experimental hypertension

I Eide, V Campese, D Stein, K Eide, V DeQuattro

PMID: 755646 DOI: 10.3109/10641967809068595

Abstract

Orthostatic changes of systolic, diastolic and pulse pressure, and pulse rates were evaluated as clinical indicators of sympathetic nerve tone in 28 patients with uncomplicated primary hypertension. After sixty minutes in the upright position, systolic blood pressure increased in 13 and decreased in 15 of the patients, while pulse pressure diminished in 19, was unchanged in 4 and increased in 5 of the patients. The changes of both systolic blood pressure and pulse pressure showed a significant positive correlation with basal (supine) levels of norepinephrine (r = 0.40, p less than 0.05 and r = 0.54, p less than 0.01, respectively). In the total sample of patients, 25% had basal plasma norepinephrine concentrations above the normal range. Of the patients with increased systolic blood pressure after standing, 38% had elevated basal norepinephrine. Similarly in patients with increased orthostatic pulse pressure or in those with pulse pressure reductions less than 10 mm Hg, 45% had elevated basal norepinephrine. On the other hand, of patients with reductions of pulse pressure of more than 10 mm Hg, only 6% had elevated basal norepinephrine. Of the patients with similar systolic blood pressure reductions, none had increased plasma norepinephrine. Both diastolic blood pressures and pulse rates always rose during orthostatic stress, but they did not correlate with basal sympathetic tone. In conclusion, hypertensive patients with orthostatic increases of systolic and pulse pressure are more likely to have elevated basal sympathetic tone than unresponsive patients. The former may comprise a subset of hypertensives who have a causal neurogenic component. They may be more sensitive to drugs which suppress sympathetic nerve function.

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