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 NG-monomethyl-⌊-arginine (⌊-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 ⌊-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.
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Research Article|
June 16 1999
Basal nitric oxide production is impaired in offspring of patients with essential hypertension
A. S. McALLISTER;
A. S. McALLISTER
*Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
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A. B. ATKINSON;
A. B. ATKINSON
*Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
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G. D. JOHNSTON;
G. D. JOHNSTON
†Department of The rapeutics and Pharmacology, The Queen's University of Belfast, Belfast BT9 7BL, Northern Ireland, U.K.
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D.R. HADDEN;
D.R. HADDEN
*Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
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P. M. BELL;
P. M. BELL
*Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
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D. R. McCANCE
*Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, U.K.
Correspondence: Dr David R. McCance.
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Publisher: Portland Press Ltd
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 1999
1999
Clin Sci (Lond) (1999) 97 (2): 141–147.
Citation
A. S. McALLISTER, A. B. ATKINSON, G. D. JOHNSTON, D.R. HADDEN, P. M. BELL, D. R. McCANCE; Basal nitric oxide production is impaired in offspring of patients with essential hypertension. Clin Sci (Lond) 1 August 1999; 97 (2): 141–147. doi: https://doi.org/10.1042/cs0970141
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