Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
2001-6-19
pubmed:abstractText
BACKGROUND:Menopause heralds a dramatic increase in incident hypertension, suggesting a protective effect of estrogen on blood pressure (BP). In female rats, estrogen has been shown to decrease sympathetic nerve discharge (SND) and BP. SND, however, has not been recorded during estrogen replacement therapy (ERT) in humans. Methods and Results-In 12 normotensive postmenopausal women, we conducted a randomized crossover placebo-controlled study to test whether chronic ERT caused a sustained decrease in SND and BP. Twenty-four-hour ambulatory BP, SND, and arterial baroreflex sensitivity were measured before and after 8 weeks of transdermal estradiol (200 microgram/d), oral conjugated estrogens (0.625 mg/d), or placebo. To test the acute effects of estrogen on SND, additional studies were performed in the same women receiving intravenous conjugated estrogens or sublingual estradiol. After 8 weeks of transdermal ERT, the basal rate of SND decreased by 30% (from 40+/-4 to 27+/-4 bursts per minute, P=0.0001) and ambulatory diastolic BP fell by 5+/-2 mm Hg (P=0.0003). In contrast, SND and BP were unaffected either by 8 weeks of oral ERT or by acute estrogen administration. Neither transdermal nor oral ERT had any effects on baroreflex sensitivity. CONCLUSIONS:In normotensive postmenopausal women, chronic transdermal ERT decreases SND without augmenting arterial baroreflexes and causes a small but statistically significant decrease in ambulatory BP. Sympathetic inhibition is evident only with chronic rather than acute estrogen administration, implying a genomic mechanism of action. Because the effects of transdermal ERT are larger than those of oral ERT, the route of administration may be an important consideration in optimizing the beneficial effects of ERT on BP and overall cardiovascular health.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1524-4539
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2903-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11413078-Action Potentials, pubmed-meshheading:11413078-Administration, Cutaneous, pubmed-meshheading:11413078-Administration, Oral, pubmed-meshheading:11413078-Administration, Sublingual, pubmed-meshheading:11413078-Baroreflex, pubmed-meshheading:11413078-Blood Pressure, pubmed-meshheading:11413078-Cross-Over Studies, pubmed-meshheading:11413078-Diastole, pubmed-meshheading:11413078-Estradiol, pubmed-meshheading:11413078-Estrogen Replacement Therapy, pubmed-meshheading:11413078-Estrogens, Conjugated (USP), pubmed-meshheading:11413078-Female, pubmed-meshheading:11413078-Humans, pubmed-meshheading:11413078-Injections, Intravenous, pubmed-meshheading:11413078-Microelectrodes, pubmed-meshheading:11413078-Middle Aged, pubmed-meshheading:11413078-Monitoring, Ambulatory, pubmed-meshheading:11413078-Postmenopause, pubmed-meshheading:11413078-Sympathetic Fibers, Postganglionic, pubmed-meshheading:11413078-Sympathetic Nervous System
pubmed:year
2001
pubmed:articleTitle
Transdermal estrogen replacement therapy decreases sympathetic activity in postmenopausal women.
pubmed:affiliation
Division of Hypertension, Donald W. Reynolds Cardiovascular Clinical Research Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, USA.
pubmed:publicationType
Journal Article, Clinical Trial, Randomized Controlled Trial, Research Support, Non-U.S. Gov't