Document Detail


Franz Volhard lecture. Increased systemic vascular resistance and primary hypertension: the expanding complexity.
MedLine Citation:
PMID:  2095384     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Polygenetic predisposition is a key factor in the multifactorial disorders of primary hypertension. It is suggested that endothelial cell abnormalities are the major factors responsible for the increase in total systemic vascular resistance that leads to an elevation in arterial blood pressure. Thus, resetting of the arterial baroreceptors could be a consequence of endothelial-mediated changes in mechano-electrical transduction in the arterial mechanoreceptors. In consequence, inhibition of the vasomotor centers would be diminished and the resulting neurohumoral excitation would constrict the systemic resistance blood vessels. Later, as left ventricular hypertrophy develops, the inhibitory input of the cardiac mechanoreceptors is also reduced. In normal endothelial cells there is a predominant formation and release of vascular smooth muscle relaxing and growth-inhibiting factors. However, it is proposed that genetic changes lead to a predominate formation of endothelium-derived contracting factors and mitogens. The former would augment the neurohumoral vasoconstriction. The latter, aided by the increased arterial pressure and the augmented output of norepinephrine, would lead to structural alterations in the arterial vessels, thus reducing the lumen area, amplifying the vasoconstrictor response to contractile agents and limiting vasodilation. In this way the hypertension would be perpetuated.
Authors:
J T Shepherd
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal of hypertension. Supplement : official journal of the International Society of Hypertension     Volume:  8     ISSN:  0952-1178     ISO Abbreviation:  J Hypertens Suppl     Publication Date:  1990 Dec 
Date Detail:
Created Date:  1991-07-08     Completed Date:  1991-07-08     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8501422     Medline TA:  J Hypertens Suppl     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  S15-27     Citation Subset:  IM; S    
Affiliation:
Mayo Clinic and Foundation, Rochester, Minnesota 55905.
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MeSH Terms
Descriptor/Qualifier:
Animals
Endothelium, Vascular / physiology
Growth Substances / physiology
Humans
Hypertension / genetics,  physiopathology*
Mechanoreceptors / physiology
Nitric Oxide / physiology
Pressoreceptors / physiology
Reflex / physiology
Sympathetic Nervous System / physiology
Vascular Resistance / physiology*
Chemical
Reg. No./Substance:
0/Growth Substances; 10102-43-9/Nitric Oxide

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


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