2001
DOI: 10.1136/heart.85.2.215
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Endothelial dysfunction in hypertensive patients and in normotensive offspring of subjects with essential hypertension

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Cited by 46 publications
(30 citation statements)
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“…2 It is also known that one of the earliest changes observed in hypertensive subjects, either in stage 1 of hypertension or in normotensive (NT) subjects with a family history of hypertension is an impaired endothelial response to reactive hyperaemia. [3][4][5][6] Previous data from our group have detected a graded impairment in vasodilatatory response from NT healthy subjects compared to smokers, hypertensive and those with hypertension and diabetes mellitus, suggesting that not only blood pressure levels but the presence or coexistence of other risk factors may decrease this vasodilatatory response. 7 Endothelial dysfunction was initially described as a lack in nitric oxide (NO) release and/or excess of free radicals, suggesting an imbalance between vasodilators and vasoconstrictor agents present at endothelial cells (functional change).…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…2 It is also known that one of the earliest changes observed in hypertensive subjects, either in stage 1 of hypertension or in normotensive (NT) subjects with a family history of hypertension is an impaired endothelial response to reactive hyperaemia. [3][4][5][6] Previous data from our group have detected a graded impairment in vasodilatatory response from NT healthy subjects compared to smokers, hypertensive and those with hypertension and diabetes mellitus, suggesting that not only blood pressure levels but the presence or coexistence of other risk factors may decrease this vasodilatatory response. 7 Endothelial dysfunction was initially described as a lack in nitric oxide (NO) release and/or excess of free radicals, suggesting an imbalance between vasodilators and vasoconstrictor agents present at endothelial cells (functional change).…”
Section: Introductionmentioning
confidence: 99%
“…1 K One of the earliest changes in hypertensive and/or normotensive subjects with family history is an impairment of endothelial function expressed as vasodilation in response to reactive hyperaemia. [3][4][5][6] What this study adds K Within 10-mm Hg interval for SBP, there was a progressive and significant reduction in vasodilatory response as blood pressure raised, of 17.3 and 14.2%, respectively. K Starting from a SBP X125 mm Hg up to a SBP o140 mm Hg there was a marked reduction in vasodilation of 29%.…”
mentioning
confidence: 99%
“…1 A number of early pathophysiologic abnormalities that precede the onset of hypertension have been observed in FH þ , including cardiac anatomical -functional alterations, 2-4 vascular dysfunction, 5,6 altered renal haemodynamics, 7 a higher density of platelet a 2 -adrenoceptors, 8 altered haemostasis, 9 and metabolic disturbances. [10][11][12][13][14] For example, one of the earliest detectable cardiac abnormalities appears to be altered left ventricular function that may precede left ventricular hypertrophy.…”
Section: Introductionmentioning
confidence: 99%
“…[10][11][12][13][14] For example, one of the earliest detectable cardiac abnormalities appears to be altered left ventricular function that may precede left ventricular hypertrophy. Endothelial dependent flow-mediated vasodilatation is impaired 6 and arterial stiffness is augmented 5 in FH þ , which may play a role in reducing baroceptor responsiveness to changes in pressure. Furthermore, FH þ are characterized by a hyperactive sympathetic nervous system that manifests during physical and mental stressors (see Figure 1).…”
Section: Introductionmentioning
confidence: 99%
“…5 Studies have found evidence of abnormal endothelial function in people with risk factors for arterial hypertension and atherosclerosis, such as obesity, familial hypercholesterolemia, family history of arterial hypertension and low birth weight. [6][7][8] These studies assessed endothelial function by means of high-resolution B-mode ultrasound, a methodology that is widely used to evaluate endotheliumdependent vascular dilatation. This dilatation is a function of NO, which is a potent vasodilator and is produced by endothelial cells in response to stimulation from blood in contact with the vessel walls.…”
Section: Introductionmentioning
confidence: 99%