The Effects of Local Intra-Arterial NG-Monomethyl L-Arginine (L-NMMA) in Hypertensive Patients: The Nitric Oxide (NO) Dilator Mechanism Appears Impaired

Calver, AL; Collier, Joe; Vallance, P.; Griffin, George E.

doi:10.1042/cs081007pc

Cited by 107 publications

(151 citation statements)

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“…We also found in the present study an inverse relationship between MAP and urinary 15 N nitrate excretion throughout the blood pressure range, a result consistent with ours 9 and other previous findings 22,23 that NO synthesis is reduced in patients with essential hypertension. Because gender and blood pressure were significantly correlated with urinary 15 N nitrate excretion, we examined the possibility that blood pressure acted as a confounding variable.…”

Section: N Nitrate After Intravenous Administration Of L-[supporting

confidence: 82%

Evidence for a Difference in Nitric Oxide Biosynthesis Between Healthy Women and Men

et al. 1998

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Abstract-There is indirect evidence for a gender difference in nitric oxide (NO) synthesis from vascular endothelium. The aim of the present study was to determine NO production more directly in healthy women and men by the measurement of 15 N nitrate excreted in urine after the intravenous administration of L-[ 15 N] 2 -guanidino arginine. Twenty-four healthy volunteers (13 men aged 22 to 40 years and 11 women aged 23 to 42 years) participated in this study. No subjects were receiving any medication. Women were studied between the 7th and 14th days of their menstrual cycles. Arterial blood pressure was measured oscillometrically, and 1.13 mol L-[ 15 N] 2 arginine was administered intravenously after an overnight fast. Urine was collected for the next 36 hours in separate 12-hour periods. Urinary 15 N/ 14 N nitrate ratio was assessed by dry combustion in an isotope ratio mass spectrometer. Mean 36-hour urinary 15 N nitrate excretion was greater in women than in men (2111Ϯ139 versus 1682Ϯ87 mol; PϽ0.05). Furthermore, total urinary 15 N nitrate excretion was associated inversely with the mean arterial blood pressure in the whole group of subjects (coefficient of correlation, 0.47; Pϭ0.022). The present data show that whole-body production of NO is greater in healthy premenopausal women than in men under ambulatory conditions. The cellular origin of NO measured in this study is unknown, but differences in endothelial production could underlie differences in vascular function between men and women. (Hypertension. 1998;32:730-734.) Key Words: endothelium-derived relaxing factor Ⅲ arginine Ⅲ nitrates Ⅲ gender Ⅲ adults P remenopausal women have less atheromatous arterial disease, including stroke or coronary artery disease, than men of similar age.1 Synthesis of nitric oxide (NO) by the endothelium regulates vascular tone in the arterial bed and modulates interactions between the endothelium and circulating blood cells, including platelets and leukocytes.2 Previous studies have suggested that a gender difference in the production of NO due to ovarian hormones (ie, estrogens) could contribute to this low risk of cardiovascular events in women of reproductive age. However, the role of NO is controversial because increased 3,4 or diminished 5,6 production in women compared with men has been reported. It is possible that the indirect nature and relative specificity of the methods used for the measurement of NO in those studies might account for these discrepancies. Measurement of urinary or serum nitrate is highly affected by diet.7 Cyclic GMP is also the second messenger of atrial natriuretic peptide, 8 and exhaled NO reflects local biosynthesis in the lung and/or upper airways rather than in the whole body. We have developed a sensitive and specific method to measure more directly the conversion of L-arginine to NO. 9 The method is based on the measurement of 15 N nitrate (stable oxidation product of NO) excretion in urine after intravenous single administration of the stable isotope L-[ 15 N] 2 -guanidino arginine. Us...

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Section: N Nitrate After Intravenous Administration Of L-[supporting

confidence: 82%

Evidence for a Difference in Nitric Oxide Biosynthesis Between Healthy Women and Men

et al. 1998

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“…Basal production of vascular NO, assessed by quantification of the vasoconstrictor responses to NOS inhibitors, has been shown to be impaired in human hypertensive subjects. 29,30 Stimulated vascular NO release (endothelial function) has also been shown to be impaired by several investigators. They demonstrated attenuated responses to endothelium depen-dent vasodilators such as acetylcholine but preserved responses to endothelium independent vasodilators such as sodium nitroprusside in hypertensive patients 31,32 and even in their normotensive offspring.…”

Section: Endothelial No and Hypertensionmentioning

confidence: 99%

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

Chowdhary

Townend

2001

J Hum Hypertens

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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-

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“…50,53,54 Decreased NOS levels in essential hypertension have been reported, as well as muted vasoconstrictor response to L-NMMA, although this is not a universal finding. 55 It should be emphasized that dysfunctional endothelium-dependent vasodilation is not merely a cause of hypertension; it exists in several disease states (as outlined here), and degree of endothelial dysfunction does not correlate with blood pressure values. 15 Hypertension plays an etiologic role in ED beyond its correlation with endothelial dysfunction.…”

Section: Hypertensionmentioning

confidence: 99%

Linking erectile dysfunction and coronary artery disease

2005

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Coronary artery disease (CAD) and erectile dysfunction (ED) are both highly prevalent conditions that frequently coexist. Additionally, they share mutual vascular risk factors, suggesting that they are both manifestations of systemic vascular disease. The role of endothelial dysfunction in CAD is well established. Normal erectile function is primarily a vascular event that relies heavily on endothelially derived, nitric oxide-induced vasodilation. Accordingly, endothelial dysfunction appears to be a common pathological etiology and mechanism of disease progression between CAD and ED. The risk factors of diabetes mellitus, hypertension, hyperlipidemia, obesity and tobacco abuse contribute to endothelial dysfunction. This article reviews the role of vascular endothelium in health, the abnormalities resulting from vascular risk factors, and clinical trials evaluating the role of endothelial dysfunction in ED.

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The Effects of Local Intra-Arterial NG-Monomethyl L-Arginine (L-NMMA) in Hypertensive Patients: The Nitric Oxide (NO) Dilator Mechanism Appears Impaired

Cited by 107 publications

References 0 publications

Evidence for a Difference in Nitric Oxide Biosynthesis Between Healthy Women and Men

Evidence for a Difference in Nitric Oxide Biosynthesis Between Healthy Women and Men

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

Linking erectile dysfunction and coronary artery disease

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