NDLI: Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kellogg, Dean L. Zhao, Joan L. Wu, Yubo
Description	Country affiliation: United States Author Affiliation: Kellogg DL ( Division of Geriatrics and Gerontology, Univ. of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. kelloggd@uthscsa.edu)
Abstract	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.
File Format	HTM / HTML
ISSN	03636135
e-ISSN	15221539
DOI	10.1152/ajpheart.00082.2008
Journal	AJP: Heart and Circulatory Physiology
Issue Number	1
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Cardiology Arginine Analogs & Derivatives Endothelium, Vascular Drug Effects Enzyme Inhibitors Pharmacology Heat Stress Disorders Physiopathology Nitric Oxide Synthase Type Iii Antagonists & Inhibitors Skin Temperature Skin Blood Supply Vasodilation Administration, Cutaneous Administration & Dosage Blood Pressure Enzymology Forearm Metabolism Laser-doppler Flowmetry Microdialysis Nitric Oxide Nitroprusside Regional Blood Flow Time Factors Vasodilator Agents Clinical Trial Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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