Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2004;44:e3-e4
Published online before print June 7, 2004, doi: 10.1161/01.HYP.0000133817.30057.2b
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
44/2/e3    most recent
01.HYP.0000133817.30057.2bv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lechin, F.
Right arrow Articles by Esler, M. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lechin, F.
Right arrow Articles by Esler, M. D.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*High Blood Pressure

(Hypertension. 2004;44:e3.)
© 2004 American Heart Association, Inc.


Letters to the Editor

Neural Sympathetic Activity in Essential Hypertension

Fuad Lechin; Bertha van der Dijs

Department of Physiological Sciences, Sections of Neurochemical, Neurophysiology, Neuroimmunology, and Neuropharmacology, Instituto de Medicina Experimental, Universidad Central de Venezuela, Caracas, Venezuela

Alex E. Lechin

Sleep Disorders Center, Memorial Herman Hospital, Houston, Tex


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

We read with great interest the article by Schlaich et al1 dealing with the issue of sympathetic augmentation in hypertension. In 1993, we demonstrated that neural sympathetic activity predominance is registered in essential hypertensive patients.2 These findings were supported by the overwhelming circulating noradrenaline (NA) versus adrenaline (Ad) levels registered throughout the oral glucose tolerance test. This NA versus Ad predominance has also been demonstrated through the supine-resting/1-minute orthostasis/5-minute moderate exercise test. This test is based on the findings of Robertson et al, who demonstrated that NA, but not Ad, peaks at 1-minute orthostasis. Thus, this test allowed the investigation of both neural and adrenal sympathetic release, separately. With respect to this, we have performed this test in some 25 000 normal and diseased subjects, and the results have been published in >50 research articles and in 3 books dealing with the autonomic nervous system.3,4 Our results might be summarized as follows: the normal NA/Ad plasma ratio is lower than 2 during the supine-resting situation. This NA/Ad ratio rises to 3 to 4 in normal subjects during 1-minute orthostasis. The NA/Ad ratio does not increase, but decreases in nonessential hypertensive and/or stressed subjects, despite the global assessment that plasma catecholamines show significant increases. Conversely, essential hypertensive patients show great NA rise but none or poor Ad rise at 1-minute orthostasis. Thus, the NA/Ad ratio shows maximal increase, reaching levels >8. Plasma dopamine (DA) values do not increase in essential hypertensive patients. Thus, the NA/DA ratio shows significant . . . [Full Text of this Article]

Markus P. Schlaich

Department of Medicine IV, University of Erlangen-Nuernberg, Erlangen, Germany

Murray D. Esler

Baker Heart Research Institute and Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia




This article has been cited by other articles:


Home page
HypertensionHome page
J. E. Hall
Hypertension Online Only: August 2004
Hypertension, August 1, 2004; 44(2): 244 - 244.
[Full Text] [PDF]