DAVID S. GOLDSTEIN, M.D., Ph.D; PAUL D. LEVINSON, M.D.; REUVEN ZIMLICHMAN, M.D.; ARTHUR PITTERMAN, M.D.; ROBIN STULL; HARRY R. KEISER, M.D.
To assess the contribution of sympathetic outflow to blood pressure in patients with essential hypertension, we measured blood pressure and plasma norepinephrine responses to clonidine, an antihypertensive agent that decreases central sympathetic outflow, in 44 patients and in 41 normotensive control subjects of similar age. Among the hypertensive patients, the resting level of plasma norepinephrine was significantly related to the decrease in mean arterial pressure 3 hours after a single oral dose of clonidine, 300µg (r=0.62, p < 0.001). The magnitude of the depressor response in the patients also was correlated significantly with the decrease in plasma norepinephrine after clonidine (r=0.60, p < 0.001). These results suggest that increased sympathetic outflow plays a pathophysiologic role in some patients with essential hypertension.
DAVID S. GOLDSTEIN, PAUL D. LEVINSON, REUVEN ZIMLICHMAN, ARTHUR PITTERMAN, ROBIN STULL, HARRY R. KEISER. Clonidine Suppression Testing in Essential Hypertension. Ann Intern Med. 1985;102:42–48. doi: 10.7326/0003-4819-102-1-42
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Published: Ann Intern Med. 1985;102(1):42-48.
Cardiology, Coronary Risk Factors, Hypertension, Nephrology.
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