Basal nitric oxide synthesis in essential hypertension

Forte, Pablo; Copland, Mhairi; Smith, Lorna; Milne, Eric; Sutherland, John C.; Benjamin, Nigel

doi:10.1016/s0140-6736(96)07631-3

Cited by 341 publications

(221 citation statements)

References 25 publications

Supporting

Mentioning

204

Contrasting

Unclassified

Order By: Relevance

“…[20][21][22] However, studies performed in humans in which Abbreviations: BMI, body mass index; BP, blood pressure; NSS, normotensive salt-sensitive subject; NSR, normotensive salt-resistant subject; UK, urine potassium excretion; Una, urine sodium excretion.…”

Section: Discussionmentioning

confidence: 99%

Endothelial dysfunction in normotensive salt-sensitive subjects

et al. 2011

J Hum Hypertens

View full text Add to dashboard Cite

Salt-sensitivity is associated with a more severe target organ injury and higher mortality, even in normotensive subjects. As endothelial dysfunction is predictive for future cardiovascular events, we evaluated whether normotensive salt-sensitive (NSS) subjects have more pronounced endothelial dysfunction compared with normotensive salt-resistant (NSR) subjects. Normotensive subjects (n ¼ 99, aged 25-50 years) were selected from a rural community in northern China. Salt sensitivity was assigned if mean BP increased by X10% from a 1-week high salt (18 g/day, NaCl) to low-salt diet (3 g/day, NaCl). Endothelial function was assessed by testing the flow-mediated dilatation (FMD) of the brachial artery using high-resolution ultrasound, as well as nitrogen oxide (NOx) levels, in plasma and urine at baseline. Blood pressure at baseline was similar between NSS and NSR subjects, but diverged during salt intervention. Furthermore, FMD was significantly lower in 17 NSS subjects (10.2 ± 2.5 vs 14.5 ± 1.6%, P ¼ 0.037) compared with NSR subjects. In addition, average plasma NOx levels were lower in NSS subjects than NSR subjects (61.2 ± 3.23 lM vs 82.5 ± 1.61 lM, P ¼ 0.034). Moreover, Both FMD and plasma NOx levels were negatively correlated with the degree of salt sensitivity (r ¼ À0.435 and r ¼ À0.459, respectively, Po0.01). However, there was no difference in urine NOx between the two groups. Our study indicates that endothelial dysfunction could contribute to the long-term higher levels of target organ injury and higher mortality observed in NSS subjects.

show abstract

Section: Discussionmentioning

confidence: 99%

Endothelial dysfunction in normotensive salt-sensitive subjects

et al. 2011

J Hum Hypertens

View full text Add to dashboard Cite

show abstract

“…18,19,29 NO is a free radical that was considered as the major endothelium-derived relaxing factor and was found to be reduced in patients with essential hypertension. [30][31][32] As this pathologic alteration becomes manifest in the earliest stage of hypertension, endothelial dysfunction may represent an initial factor predisposing to atherogenesis. 10 In recent studies, plasma NO levels were evaluated also in WCH as an indicator of endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Increased circulating concentrations of asymmetric dimethylarginine (ADMA) in white coat hypertension

et al. 2005

View full text Add to dashboard Cite

Elevated plasma levels of the endogenous nitric oxide (NO) synthase inhibitor asymmetric dimethylarginine (ADMA) contribute to endothelial dysfunction and seem to be a predictor for cardiovascular mortality. Elevated ADMA plasma concentrations have been demonstrated in patients with hypertension. However, the plasma concentrations of ADMA in white coat hypertension (WCH) has not been previously studied. The aim of this study was to evaluate ADMA in WCH and compare with normotensive (NT) and hypertensive (HT) patients. We also evaluated the relation between ADMA and NO in these three groups. For this purpose, 34 NT, 34 white coat hypertensive (clinical hypertension and ambulatory daytime blood pressure o135/85 mmHg) and 34 HT patients were recruited in this study. The subjects were matched for age, gender, body mass index (BMI) and the patients with smoking habit, dyslipidaemia and diabetes mellitus were excluded. The ADMA levels were determined by high performance liquid chromatography. Plasma ADMA levels were significantly higher in WCH group than in the NT group (3.2170.49 lmol/l vs 2.8470.58 lmol/l, P ¼ 0.046). It was significantly higher in the HT group than in the NTs (4.2470.38 lmol/l, Po0.001). There was also a significant difference between the HT and WCH groups (Po0.001). The WCH subjects had significantly higher levels of NO than the HTs (41.6872.23 vs 32.1872.68 lmol/l; Po0.001) and significantly lower values than the NTs (48.247 4.29 lmol/l; Po0.001). In WCH and HT group, there was a negative correlation between ADMA and NO (r ¼ À0.515, P ¼ 0.003 and r ¼ À0.389, P ¼ 0.034, respectively). In NT subjects, there was no correlation between these two parameters (r ¼ À0.287, P ¼ 0.124). The correlation between ADMA and NO was stronger in WCH group than in HT group. Although NO levels in HT patients were lower than WCHs and ADMA levels were higher in HT patients than WCHs, the negative correlation of these two parameters were more pronounced in WCH group. Decreased NO and increased ADMA levels in WCH may indicate endothelial dysfunction. Our data indicate also that WCH represent an intermediate group between NT and HT when endothelial dysfunction is concerned.

show abstract

“…Studies using radio-labelled L-arginine have shown a reduction in total body NO production in human hypertension. 39 The possibility therefore exists that a relative lack of NO activity elsewhere in the body may contribute to the pathogenesis of hypertension.…”

Section: Endothelial No and Hypertensionmentioning

confidence: 99%

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Chowdhary

Townend

2001

J Hum Hypertens

View full text Add to dashboard Cite

The importance of endothelial nitric oxide (NO) generation in sustaining a tonic systemic vasodilatation is well established. Inhibiting NO production produces hypertension in animals and in humans and not surprisingly there has been considerable interest in establishing whether deficiencies of endothelial NO pathway activity are implicated in the aetiology of essential hypertension. The results of these investigations have been inconsistent with some suggestion that observed deficiencies of both basal and stimulated endothelial NO generation in hypertensive subjects may be an effect rather than the cause of raised arterial pressure. It is increasingly recognised that neuronal production of NO also influences cardiovascular homeostasis through its action as a neuromodulator within the autonomic nervous system. Overall NO has been shown to have sym-

show abstract

Basal nitric oxide synthesis in essential hypertension

Cited by 341 publications

References 25 publications

Endothelial dysfunction in normotensive salt-sensitive subjects

Endothelial dysfunction in normotensive salt-sensitive subjects

Increased circulating concentrations of asymmetric dimethylarginine (ADMA) in white coat hypertension

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Contact Info

Product

Resources

About