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Basal nitric oxide synthesis in essential hypertension.
Lancet. 1997 Mar 22; 349(9055):837-42.Lct

Abstract

BACKGROUND

There is indirect evidence that nitric oxide (NO) synthesis in vascular endothelium of patients with hypertension is altered. The aim of this study was to estimate more directly NO production in patients with untreated essential hypertension by measurement of synthesis of inorganic nitrate, which is the end product of NO oxidation in humans. Two separate studies were undertaken in patients with hypertension and appropriate healthy controls.

METHODS

In the first study, ten patients and 13 controls were given a diet containing 82 mumoles nitrate per day for 2 days, with urinary and plasma nitrate measurement and 24 h ambulatory blood pressure monitoring on the 2nd day. In the second study, 11 patients and 11 controls were studied in the postabsorptive state; a bolus of 200 mg L[15N]2 arginine was administered intravenously over 10 min. 24 h ambulatory blood pressure monitoring was done and complete urine collections were made for the next 36 h.

FINDINGS

In the first study, 24 h urinary nitrate excretion was lower in the hypertensive patients than in the control group (mean 450 [SEM 37] vs 760 mumoles [77] per 24 h; p < 0.001). There was an inverse correlation between average mean daytime ambulatory blood pressure and nitrate excretion (p = 0.007; r2 = -0.73). In the second study, mean 36 h urinary 15N nitrate excretion was significantly lower in the hypertensive than in the control group (1313 [50] vs 2133 [142] pmoles; p < 0.001). There was an inverse correlation also between average mean daytime ambulatory blood pressure and 24 h urinary 15N nitrate excretion expressed per mmole of creatinine (p = 0.002, r2 = -0.59). In addition, total urinary 15N nitrate excretion in the hypertensive group was significantly higher in women than in men (285 [16] vs 198 [14] micrograms 15N nitrate per kg; p = 0.026).

INTERPRETATION

These data suggest that whole-body NO production in patients with essential hypertension is diminished under basal conditions. The origin of the NO we measured is not known, and we cannot tell whether the impaired synthesis is primary or secondary to a rise in blood pressure.

Authors+Show Affiliations

Department of Clinical Pharmacology, St Bartholomew's, London, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9121259

Citation

Forte, P, et al. "Basal Nitric Oxide Synthesis in Essential Hypertension." Lancet (London, England), vol. 349, no. 9055, 1997, pp. 837-42.
Forte P, Copland M, Smith LM, et al. Basal nitric oxide synthesis in essential hypertension. Lancet. 1997;349(9055):837-42.
Forte, P., Copland, M., Smith, L. M., Milne, E., Sutherland, J., & Benjamin, N. (1997). Basal nitric oxide synthesis in essential hypertension. Lancet (London, England), 349(9055), 837-42.
Forte P, et al. Basal Nitric Oxide Synthesis in Essential Hypertension. Lancet. 1997 Mar 22;349(9055):837-42. PubMed PMID: 9121259.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Basal nitric oxide synthesis in essential hypertension. AU - Forte,P, AU - Copland,M, AU - Smith,L M, AU - Milne,E, AU - Sutherland,J, AU - Benjamin,N, PY - 1997/3/22/pubmed PY - 1997/3/22/medline PY - 1997/3/22/entrez SP - 837 EP - 42 JF - Lancet (London, England) JO - Lancet VL - 349 IS - 9055 N2 - BACKGROUND: There is indirect evidence that nitric oxide (NO) synthesis in vascular endothelium of patients with hypertension is altered. The aim of this study was to estimate more directly NO production in patients with untreated essential hypertension by measurement of synthesis of inorganic nitrate, which is the end product of NO oxidation in humans. Two separate studies were undertaken in patients with hypertension and appropriate healthy controls. METHODS: In the first study, ten patients and 13 controls were given a diet containing 82 mumoles nitrate per day for 2 days, with urinary and plasma nitrate measurement and 24 h ambulatory blood pressure monitoring on the 2nd day. In the second study, 11 patients and 11 controls were studied in the postabsorptive state; a bolus of 200 mg L[15N]2 arginine was administered intravenously over 10 min. 24 h ambulatory blood pressure monitoring was done and complete urine collections were made for the next 36 h. FINDINGS: In the first study, 24 h urinary nitrate excretion was lower in the hypertensive patients than in the control group (mean 450 [SEM 37] vs 760 mumoles [77] per 24 h; p < 0.001). There was an inverse correlation between average mean daytime ambulatory blood pressure and nitrate excretion (p = 0.007; r2 = -0.73). In the second study, mean 36 h urinary 15N nitrate excretion was significantly lower in the hypertensive than in the control group (1313 [50] vs 2133 [142] pmoles; p < 0.001). There was an inverse correlation also between average mean daytime ambulatory blood pressure and 24 h urinary 15N nitrate excretion expressed per mmole of creatinine (p = 0.002, r2 = -0.59). In addition, total urinary 15N nitrate excretion in the hypertensive group was significantly higher in women than in men (285 [16] vs 198 [14] micrograms 15N nitrate per kg; p = 0.026). INTERPRETATION: These data suggest that whole-body NO production in patients with essential hypertension is diminished under basal conditions. The origin of the NO we measured is not known, and we cannot tell whether the impaired synthesis is primary or secondary to a rise in blood pressure. SN - 0140-6736 UR - https://www.unboundmedicine.com/medline/citation/9121259/Basal_nitric_oxide_synthesis_in_essential_hypertension_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0140-6736(96)07631-3 DB - PRIME DP - Unbound Medicine ER -