@article{5f1fa71e2bdb42c6ae8b194c7b2ca310,
title = "Pharmacologic and tracer methods to study sympathetic function in primary hypertension",
abstract = "Systemically infused tritiated norepinephrine (NE) was used to estimate total body NE spillover into arterial blood during mental challenge (playing a video game) in 18 young (mean age 35 years old) patients with essential hypertension and 20 normotensives of similar age. Arterial NE, epinephrine (E), and total body NE spillover at baseline did not differ between the groups. During the game, total body NE spillover increased significantly in both groups, with the increments related directly to the pressor responses. Mean increments in total body NE spillover, arterial E, and mean arterial pressure were larger in the hypertensives (204 vs 91 ng/min, 33 vs 9 pg/ml, and 16 vs 12 mm Hg). The hypertensives increased total peripheral resistance during the game, whereas the normotensive group did not. Intravenous administration of yohimbine was used to increase NE spillover. Pressor responses to yohimbine were related to responses of arterial NE. The hypertensive group had a larger mean increment in blood pressure and arterial NE than did the normotensive group during yohimbine, due to excessive responses in a subgroup of about 1/3 of the patients. Patients with essential hypertension can have excessive sympathoadrenomedullary responsiveness related to excessive pressor responses, even when sympathoadrenomedullary activity at rest is normal.",
keywords = "Epinephrine, Hypertension, Norepinephrine, Stress, Sympathetic nervous system",
author = "Goldstein, {David S.} and Graeme Eisenhofer and Moshe Garty and Sax, {Frederic L.} and Keiser, {Harry R.} and Kopin, {Irwin J.} and Folio, {Carol Joan} and Robin Stull and Bert Chidakel",
note = "Funding Information: In conclusion, the present results suggest that patients with essential hypertension can have abnormal sympathoadrenomedullary responsiveness and augmented neurogenic pressor responses without abnormalities noted at rest and without excessive pressor responses for a given amount of endogenous agonist release. Acknowledgement: Dr. Eisenhofer was supported by an International Research Fellowship of the United States Public Health Service.",
year = "1989",
doi = "10.3109/10641968909045422",
language = "אנגלית",
volume = "A11",
pages = "173--189",
journal = "Clinical and Experimental Hypertension",
issn = "1064-1963",
publisher = "Taylor and Francis Ltd.",
number = "S1",
}