Document Detail


Role of estrogen in nitric oxide- and prostaglandin-dependent modulation of vascular conductance during treadmill locomotion in rats.
MedLine Citation:
PMID:  15247204     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Endothelial production of nitric oxide (NO) and prostaglandins (PG) may be greater in females than in males, increasing vasodilatory responses in females. Does sex influence the cardiovascular responses to dynamic exercise through estrogen-dependent modulation of NO and PG vasodilatory pathways? After the administration of hexamethonium, we assessed terminal aortic blood flow (TAQ), mean arterial pressure (MAP), and hindlimb vascular conductance (VC) in four groups of rats (6 males, 5 females, 5 ovariectomized females, and 6 ovariectomized females with chronic estrogen supplementation) during graded mild-intensity treadmill locomotion (5-15 m/min, 0 degrees grade, 2 min). All rats repeated exercise after cyclooxygenase inhibition (indomethacin) and then again after NO synthase inhibition (nitro-l-arginine methyl ester) to examine the roles of NO and PG. Regression analysis was used to determine the influence of sex and plasma 17beta-estradiol on TAQ, MAP, and VC. The analysis revealed that female sex did not influence TAQ but reduced MAP and increased VC at rest and during exercise conditions. Plasma 17beta-estradiol (measured by immunoassay) significantly decreased MAP and increased TAQ and VC, irrespective of sex. Cyclooxygenase inhibition eliminated the significant association between MAP and estrogen, suggesting that estrogenic modulation occurred through PG-dependent processes. In contrast, the significant influence of estrogen on TAQ and VC was eliminated after NO synthase inhibition. On the basis of the overall findings of this study, estrogen influenced the vascular responses to dynamic exercise through PG- and NO-dependent pathways, but this occurred independent of sex.
Authors:
Jennifer Rogers; Don D Sheriff
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  97     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-12     Completed Date:  2005-01-14     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  756-63     Citation Subset:  IM    
Affiliation:
Department of Exercise Science, University of Iowa, Iowa City, IA 52242, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antihypertensive Agents / pharmacology
Blood Pressure / drug effects,  physiology
Cyclooxygenase Inhibitors / pharmacology
Enzyme Inhibitors / pharmacology
Estrogens / pharmacology,  physiology*
Female
Hexamethonium / pharmacology
Hindlimb / blood supply
Hyperemia / metabolism,  physiopathology
Indomethacin / pharmacology
Male
Motor Activity / physiology*
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / metabolism*
Ovariectomy
Prostaglandins / metabolism*
Rats
Rats, Sprague-Dawley
Regional Blood Flow / physiology*
Grant Support
ID/Acronym/Agency:
HL-46314/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Cyclooxygenase Inhibitors; 0/Enzyme Inhibitors; 0/Estrogens; 0/Prostaglandins; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 53-86-1/Indomethacin; 60-26-4/Hexamethonium

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


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