Document Detail


Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo.
MedLine Citation:
PMID:  18469149     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nitric oxide (NO) participates in locally mediated vasodilation induced by increased local skin temperature (T(loc)) and in sympathetically mediated vasodilation during whole body heat stress. We hypothesized that endothelial NOS (eNOS) participates in the former, but not the latter, response. We tested this hypothesis by examining the effects of the eNOS antagonist N(G)-amino-l-arginine (l-NAA) on skin blood flow (SkBF) responses to increased T(loc) and whole body heat stress. Microdialysis probes were inserted into forearm skin for drug delivery. One microdialysis site was perfused with l-NAA in Ringer solution and a second site with Ringer solution alone. SkBF [laser-Doppler flowmetry (LDF)] and blood pressure [mean arterial pressure (MAP)] were monitored, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF / MAP). In protocol 1, T(loc) was controlled with LDF/local heating units. T(loc) initially was held at 34 degrees C and then increased to 41.5 degrees C. In protocol 2, after a normothermic period, whole body heat stress was induced (water-perfused suits). At the end of both protocols, 58 mM sodium nitroprusside was perfused at both microdialysis sites to cause maximal vasodilation for data normalization. In protocol 1, CVC at 34 degrees C T(loc) did not differ between l-NAA-treated and untreated sites (P > 0.05). Local skin warming to 41.5 degrees C T(loc) increased CVC at both sites. This response was attenuated at l-NAA-treated sites (P < 0.05). In protocol 2, during normothermia, CVC did not differ between l-NAA-treated and untreated sites (P > 0.05). During heat stress, CVC rose to similar levels at l-NAA-treated and untreated sites (P > 0.05). We conclude that eNOS is predominantly responsible for NO generation in skin during responses to increased T(loc), but not during reflex responses to whole body heat stress.
Authors:
Dean L Kellogg; Joan L Zhao; Yubo Wu
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, N.I.H., Extramural     Date:  2008-05-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  295     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-07-15     Completed Date:  2008-08-21     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H123-9     Citation Subset:  IM    
Affiliation:
Division of Geriatrics and Gerontology, Univ. of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. kelloggd@uthscsa.edu
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MeSH Terms
Descriptor/Qualifier:
Administration, Cutaneous
Adult
Arginine / administration & dosage,  analogs & derivatives*,  pharmacology
Blood Pressure / drug effects
Endothelium, Vascular / drug effects*,  enzymology
Enzyme Inhibitors / administration & dosage,  pharmacology*
Female
Forearm
Heat Stress Disorders / metabolism,  physiopathology*
Humans
Laser-Doppler Flowmetry
Male
Microdialysis
Nitric Oxide / metabolism
Nitric Oxide Synthase Type III / antagonists & inhibitors*,  metabolism
Nitroprusside / pharmacology
Regional Blood Flow / drug effects
Skin / blood supply*
Skin Temperature*
Time Factors
Vasodilation / drug effects*
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
HL-065599/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 57444-72-1/N(G)-aminoarginine; 74-79-3/Arginine; EC 1.14.13.39/NOS3 protein, human; EC 1.14.13.39/Nitric Oxide Synthase Type III
Comments/Corrections

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