Document Detail


Basal nitric oxide production is impaired in offspring of patients with essential hypertension.
MedLine Citation:
PMID:  10409468     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There is considerable evidence that endothelium-dependent nitric oxide (NO)-mediated vasodilatation in response to acetylcholine is impaired in essential hypertension, whereas the endothelium-independent response to sodium nitroprusside is normal. More limited data have suggested that there is also reduced vasoconstriction in response to N(G)-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of basal NO release. As it is not known whether endothelial dysfunction in hypertension, if indeed present, is a cause or consequence of the condition, we have studied the normotensive offspring of parents with essential hypertension. Both basal and stimulated vascular responses were examined in 12 normotensive offspring [mean age (+/-S.E.M.) 26.1+/-1.4 years] of parents with essential hypertension and compared with those in 12 age-matched offspring (mean age 25.6+/-1.1 years) of normotensive subjects. Forearm blood flow was measured simultaneously in both arms by venous occlusion plethysmography, both at baseline and during intra-arterial brachial infusion of increasing doses of acetylcholine, sodium nitroprusside, noradrenaline and L-NMMA. There were no significant differences between the groups in the responses to acetylcholine, sodium nitroprusside or noradrenaline. In contrast, the vasoconstrictor response to L-NMMA was significantly blunted in the offspring of hypertensive parents compared with that in the offspring of normotensive parents (P=0.005). Thus endothelial dysfunction, as demonstrated by impaired basal production of NO, is present in subjects at high risk of essential hypertension, and does not occur simply as a consequence of the condition.
Authors:
A S McAllister; A B Atkinson; G D Johnston; D R Hadden; P M Bell; D R McCance
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  97     ISSN:  0143-5221     ISO Abbreviation:  Clin. Sci.     Publication Date:  1999 Aug 
Date Detail:
Created Date:  1999-10-12     Completed Date:  1999-10-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  141-7     Citation Subset:  IM    
Affiliation:
Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Adult
Endothelium, Vascular / drug effects,  metabolism
Enzyme Inhibitors / pharmacology
Female
Forearm / blood supply
Humans
Hypertension / genetics,  metabolism*
Male
Nitric Oxide / biosynthesis*
Nitroprusside / pharmacology
Norepinephrine / pharmacology
Plethysmography
Regional Blood Flow / drug effects
Vasoconstrictor Agents / pharmacology
Vasodilator Agents / pharmacology
omega-N-Methylarginine / pharmacology
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 17035-90-4/omega-N-Methylarginine; 51-41-2/Norepinephrine; 51-84-3/Acetylcholine

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


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