Document Detail

Sympathetic activation and nitric oxide function in early hypertension.
MedLine Citation:
PMID:  22287587     Owner:  NLM     Status:  MEDLINE    
The purpose of this study was to determine if tonic restrain of blood pressure by nitric oxide (NO) is impaired early in the development of hypertension. Impaired NO function is thought to contribute to hypertension, but it is not clear if this is explained by direct effects of NO on vascular tone or indirect modulation of sympathetic activity. We determined the blood pressure effect of NO synthase inhibition with N(ω)-monomethyl-l-arginine (L-NMMA) during autonomic blockade with trimethaphan to eliminate baroreflex buffering and NO modulation of autonomic tone. In this setting, impaired NO modulation of vascular tone would be reflected as a blunted pressor response to L-NMMA. We enrolled a total of 66 subjects (39 ± 1.3 yr old, 30 females), 20 normotensives, 20 prehypertensives (blood pressure between 120/80 and 140/90 mmHg), 17 hypertensives, and 9 smokers (included as "positive" controls of impaired NO function). Trimethaphan normalized blood pressure in hypertensives, suggesting increased sympathetic tone contributing to hypertension. In contrast, L-NMMA produced similar increases in systolic blood pressure in normal, prehypertensive, and hypertensive subjects (31 ± 2, 32 ± 2, and 30 ± 3 mmHg, respectively), whereas the response of smokers was blunted (16 ± 5 mmHg, P = 0.012). Our results suggest that sympathetic activity plays a role in hypertension. NO tonically restrains blood pressure by ∼30 mmHg, but we found no evidence of impaired modulation by NO of vascular tone contributing to the early development of hypertension. If NO deficiency contributes to hypertension, it is likely to be through its modulation of the autonomic nervous system, which was excluded in this study.
Alfredo Gamboa; Luis E Okamoto; André Diedrich; Leena Choi; David Robertson; Ginnie Farley; Sachin Paranjape; Italo Biaggioni
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-01-27
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  302     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-04-02     Completed Date:  2012-05-15     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1438-43     Citation Subset:  IM    
Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA.
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MeSH Terms
Aging / physiology
Baroreflex / drug effects
Blood Pressure / drug effects,  physiology
Enzyme Inhibitors / pharmacology
Heart Rate / drug effects
Hypertension / physiopathology*
Middle Aged
Muscle Tonus / drug effects,  physiology
Muscle, Smooth, Vascular / drug effects,  physiology
Nicotinic Antagonists / pharmacology
Nitric Oxide / physiology*
Nitric Oxide Synthase Type III / antagonists & inhibitors
Receptors, Nicotinic / drug effects
Smoking / physiopathology
Sympathetic Nervous System / drug effects,  physiopathology*
Trimethaphan / pharmacology
Young Adult
omega-N-Methylarginine / pharmacology
Grant Support
K23 HL-95905/HL/NHLBI NIH HHS; K23 HL095905/HL/NHLBI NIH HHS; M01 RR-000095-477450/RR/NCRR NIH HHS; P01 HL-056693-080003/HL/NHLBI NIH HHS; R01 HL-67232/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Nicotinic Antagonists; 0/Receptors, Nicotinic; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 7187-66-8/Trimethaphan; EC Oxide Synthase Type III

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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