The loss of endothelium-dependent vascular relaxation in hypertension.

Lockette, Warren; Otsuka, Yuji; Carretero, Oscar A.

doi:10.1161/01.hyp.8.6_pt_2.ii61

Cited by 302 publications

(157 citation statements)

References 9 publications

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“…16,17 Our recent studies indicate that endothelin-1 (ET-1) plays an important role in NADPH oxidase-derived O 2 Ϫ production in this model. [13][14][15] However, the interaction between ET-1-induced O 2 Ϫ and BH 4 on endothelial dysfunction and the underlying mechanisms are unknown.…”

Section: T Etrahydrobiopterin (Bhmentioning

confidence: 88%

Gene Transfer of Human Guanosine 5′-Triphosphate Cyclohydrolase I Restores Vascular Tetrahydrobiopterin Level and Endothelial Function in Low Renin Hypertension

et al. 2003

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Background-We recently reported that arterial superoxide (O 2Ϫ ) is augmented by increased endothelin-1 (ET-1) in deoxycorticosterone acetate (DOCA)-salt hypertension, a model of low renin hypertension. Tetrahydrobiopterin (BH 4 ), a potent reducing molecule with antioxidant properties and an essential cofactor for endothelial nitric oxide synthase, protects against O 2 Ϫ -induced vascular dysfunction. However, the interaction between O 2 Ϫ and BH 4 on endothelial function and the underlying mechanisms are unknown. Methods and Results-The present study tested the hypothesis that BH 4 deficiency due to ET-1-induced O 2 Ϫ leads to impaired endothelium-dependent relaxation and that gene transfer of human guanosine 5Ј-triphosphate (GTP) cyclohydrolase I (GTPCH I), the first and rate-limiting enzyme for BH 4 biosynthesis, reverses such deficiency and endothelial dysfunction in carotid arteries of DOCA-salt rats. There were significantly increased arterial O 2 Ϫ levels and decreased GTPCH I activity and BH 4 levels in DOCA-salt compared with sham rats. Treatment of arteries of DOCA-salt rats with the selective ET A receptor antagonist ABT-627, NADPH oxidase inhibitor apocynin, or superoxide dismutase (SOD) mimetic tempol abolished O 2 Ϫ and restored BH 4 levels. Basal arterial NO release and endothelium-dependent relaxations were impaired in DOCA-salt rats, conditions that were improved by apocynin or tempol treatment. Gene transfer of GTPCH I restored arterial GTPCH I activity and BH 4 levels, resulting in reduced O 2 Ϫ and improved endothelium-dependent relaxation and basal NO release in DOCA-salt rats. Conclusions-These

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Section: T Etrahydrobiopterin (Bhmentioning

confidence: 88%

Gene Transfer of Human Guanosine 5′-Triphosphate Cyclohydrolase I Restores Vascular Tetrahydrobiopterin Level and Endothelial Function in Low Renin Hypertension

et al. 2003

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“…For example, in hypercholesterolemic rabbits with impaired endothelial relaxation, NO bioavailability was decreased because of oxidation of NO into vasoinactive nitrates/nitrites, and treatment with SOD reversed endothelial dysfunction (225). Other animal models also demonstrate increased degradation of NO as the cause of endothelial dysfunction and hypertension (192). eNOS is a cytochrome p450 reductase-like enzyme that catalyzes flavin-mediated electron transport from the electron donor NAD(P)H to a prosthetic heme group.…”

Section: High Saltmentioning

confidence: 99%

Redox Control of Renal Function and Hypertension

Nistala

Whaley‐Connell

Sowers

2008

Antioxidants & Redox Signaling

139

123

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“…Lockette et al (1986) reported that endothelium-dependent responses could be 'normalized' in aortic rings of hypertensive rats after lowering of blood pressure. This argument is probably not applicable in our study because the blood pressure changes were relatively small.…”

Section: Plasma Electrolytesmentioning

confidence: 99%

Study of mechanisms of glucocorticoid hypertension in rats: endothelial related changes and their amelioration by dietary fish oils

Yin

Chu

Beilin

1992

British J Pharmacology

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1 To investigate possible mechanisms of increased systolic blood pressure after 1 weeks treatment with dexamethasone and its amelioration by fish oil feeding, we have examined the reactivity of aortic rings and perfused mesenteric resistance vessels. 2 Thirty six Sprague-Dawley rats were initially divided into two groups and fed a semisynthetic diet containing either (10% by weight) hydrogenated coconut oil and safflower oil mixture (HCO/S) (24 rats) or fish oil (12 rats) for 5 weeks. From the end of the fourth week, dexamethasone (1.25 mg ml-') in drinking water, was given to half the rats on hydrogenated coconut oil (HCO/S + Dex) and to the fish oil-fed group (fish oil + Dex). 3 One week of dexamethasone treatment raised systolic blood pressure in the HCO/S + Dex rats but not in the fish oil + Dex group. 4 Endothelium-dependent relaxation to acetylcholine (ACh) was decreased in aortic rings taken from HCO/S + Dex rats compared to rats on HCO/S alone. Relaxant responses to ACh of aortic rings from rats given fish oil + Dex were intermediate between the three groups. Aortic endothielium-independent responses to sodium nitroprusside (SNP) were unchanged between the groups, while aortic contractile responses to noradrenaline were similar in all the groups. 5 In the perfused mesenteric resistance artery, sensitivity to noradrenaline was decreased in rats given fish oil and dexamethasone compared to the other two groups. There were no differences in resistance vessel relaxation to ACh or SNP between groups. 6 Serum corticosterone levels, used as a marker of dexamethasone absorption, were substantially suppressed in dexamethasone-treated rats but levels were higher in rats on fish oil than on HCO/S diets. 7 We suggest that the glucocorticoid-induced rise in systolic blood pressure may be due in part to decreased aortic compliance as a consequence of impaired endothelium-dependent relaxation and perhaps reduced nitric oxide synthesis. Fish oil feeding may ameliorate this rise in blood pressure through (i) changes in dexamethasone absorption, (ii) decrease in reactivity to noradrenaline of perfused mesenteric resistance arteries, (iii) an increase in endothelium-dependent relaxation to ACh or a combination of these three factors.

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The loss of endothelium-dependent vascular relaxation in hypertension.

Cited by 302 publications

References 9 publications

Gene Transfer of Human Guanosine 5′-Triphosphate Cyclohydrolase I Restores Vascular Tetrahydrobiopterin Level and Endothelial Function in Low Renin Hypertension

Gene Transfer of Human Guanosine 5′-Triphosphate Cyclohydrolase I Restores Vascular Tetrahydrobiopterin Level and Endothelial Function in Low Renin Hypertension

Redox Control of Renal Function and Hypertension

Study of mechanisms of glucocorticoid hypertension in rats: endothelial related changes and their amelioration by dietary fish oils

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