Document Detail


Pregnancy and the endocrine regulation of the baroreceptor reflex.
MedLine Citation:
PMID:  20504907     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The purpose of this review is to delineate the general features of endocrine regulation of the baroreceptor reflex, as well as specific contributions during pregnancy. In contrast to the programmed changes in baroreflex function that occur in situations initiated by central command (e.g., exercise or stress), the complex endocrine milieu often associated with physiological and pathophysiological states can influence the central baroreflex neuronal circuitry via multiple sites and mechanisms, thereby producing varied changes in baroreflex function. During pregnancy, baroreflex gain is markedly attenuated, and at least two hormonal mechanisms contribute, each at different brain sites: increased levels of the neurosteroid 3alpha-hydroxy-dihydroprogesterone (3alpha-OH-DHP), acting in the rostral ventrolateral medulla (RVLM), and reduced actions of insulin in the forebrain. 3alpha-OH-DHP appears to potentiate baroreflex-independent GABAergic inhibition of premotor neurons in the RVLM, which decreases the range of sympathetic nerve activity that can be elicited by changes in arterial pressure. In contrast, reductions in the levels or actions of insulin in the brain blunt baroreflex efferent responses to increments or decrements in arterial pressure. Although plasma levels of angiotensin II are increased in pregnancy, this is not responsible for the reduction in baroreflex gain, although it may contribute to the increased level of sympathetic nerve activity in this condition. How these different hormonal effects are integrated within the brain, as well as possible interactions with additional potential neuromodulators that influence baroreflex function during pregnancy and other physiological and pathophysiological states, remains to be clearly delineated.
Authors:
Virginia L Brooks; Roger A L Dampney; Cheryl M Heesch
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-05-26
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  299     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-03     Completed Date:  2010-09-08     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R439-51     Citation Subset:  IM    
Affiliation:
Dept. of Physiology and Pharmacology, L-334, Oregon Health & Science Univ., 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. brooksv@ohsu.edu
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism
Animals
Baroreflex*
Blood Pressure
Cardiovascular System / innervation*
Endocrine System / metabolism*
Female
Heart Rate
Humans
Hydroxyprogesterones / metabolism
Insulin / metabolism
Insulin Resistance
Medulla Oblongata / metabolism
Neural Pathways / metabolism
Nitric Oxide / metabolism
Pregnancy
Pregnancy Complications / metabolism,  physiopathology
Prosencephalon / metabolism
Sympathetic Nervous System / metabolism*
Grant Support
ID/Acronym/Agency:
HL 36245/HL/NHLBI NIH HHS; HL088552/HL/NHLBI NIH HHS; HL70962/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Hydroxyprogesterones; 0/Insulin; 10102-43-9/Nitric Oxide; 11128-99-7/Angiotensin II
Comments/Corrections

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


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