Document Detail


Inhibition of nitric oxide synthase evokes central sympatho-excitation in healthy humans.
MedLine Citation:
PMID:  19723781     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Animal studies have indicated that nitric oxide is a key signalling molecule involved in the tonic restraint of central sympathetic outflow from the brainstem. Extension of these findings to humans has been difficult because systemic infusion of nitric oxide synthase (NOS) inhibitors increases blood pressure due to inhibition of endothelial NOS, resulting in activation of the arterial baroreflex and subsequent inhibition of central sympathetic outflow. To overcome this confounding inhibitory influence of the baroreflex, in the current study we directly measured skin sympathetic nerve activity (SNA), which is not under baroreceptor control. Healthy, normotensive humans were studied before, during a 60 min intravenous infusion of the NOS inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME; 4 mg kg(1)), and for 120 min following the infusion (i.e. 180 min total). Skin SNA and arterial blood pressure (BP) were continuously measured. BP was increased from baseline at the end of the l-NAME infusion (14 +/- 2 mmHg; P < 0.05) and remained significantly elevated for the remainder of the experiment (18 +/- 3 mmHg; P < 0.05). Similarly, systemic NOS inhibition produced time-dependent increases in skin SNA, such that skin SNA was elevated at the end of the l-NAME infusion (total activity, 200 +/- 22% baseline; P = 0.08) and was further increased at the end of the study protocol (total activity, 350 +/- 41% baseline; P < 0.05). Importantly, skin SNA remained unchanged during time and hypertensive (phenylephrine) control experiments. These findings indicate that pharmacological inhibition of NOS causes sympathetic activation and support a role of nitric oxide in central sympathetic control in humans.
Authors:
Colin N Young; James P Fisher; Kevin M Gallagher; Adam Whaley-Connell; Kunal Chaudhary; Ronald G Victor; Gail D Thomas; Paul J Fadel
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-09-01
Journal Detail:
Title:  The Journal of physiology     Volume:  587     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-15     Completed Date:  2010-02-03     Revised Date:  2010-10-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  4977-86     Citation Subset:  IM    
Affiliation:
Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Pressure / drug effects
Central Nervous System / drug effects,  enzymology*
Enzyme Inhibitors / administration & dosage
Female
Humans
Hypertension / enzymology
Infusions, Intravenous
Male
NG-Nitroarginine Methyl Ester / administration & dosage
Nitric Oxide / metabolism
Nitric Oxide Synthase / antagonists & inhibitors*,  metabolism
Skin / drug effects,  innervation,  metabolism
Sympathetic Nervous System / drug effects,  enzymology*
Grant Support
ID/Acronym/Agency:
DK076636/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase

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


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