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l-Arginine Depletion in Preeclampsia Orients Nitric Oxide Synthase Toward Oxidant Species
- Marina Noris,
- Marta Todeschini,
- Paola Cassis,
- Fabio Pasta,
- Anna Cappellini,
- Samantha Bonazzola,
- Daniela Macconi,
- Raffaella Maucci,
- Francesca Porrati,
- Ariela Benigni,
- Claudio Picciolo and
- Giuseppe Remuzzi
Hypertension Volume 43, Issue 31 March 2004

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Less nitric oxide (NO)-dependent vasodilation and excess formation of reactive oxygen species could explain poor placenta perfusion in preeclampsia, but the pathways involved are unknown. We tested the hypothesis that reduced NO activity and increased oxidative stress in preeclamptic placenta is related to a low bioavailability of l-arginine. Placental endothelial NO synthase (ecNOS) expression (by immunoperoxidase) and activity (by diaphorase and [³H]L-citrulline formation) were comparable in normotensive pregnancy and in preeclampsia, whereas nitrotyrosine staining, a marker of peroxynitrite, was stronger in preeclamptic villi, confirming previously reported data. Oxidative tissue damage was documented in preeclamptic villi by strong 4-hydroxynonenal-lysine staining (by immunoperoxidase), which closely colocalized with nitrotyrosine. Concentration of the NO precursor l-arginine (by HPLC) in umbilical blood and in villous tissue was lower in preeclampsia than in normotensive pregnancy. This was not caused by a defective l-arginine transport, because gene expression of the CAT-1, 4F2hc, and LAT-1 cationic amino acid transporters (by real-time reverse-transcription polymerase chain reaction [RT-PCR]) was normal. Instead, gene expression (by real-time RT-PCR) and protein tissue content (by immunoperoxidase and Western blot) of arginase II—the enzyme that degrades arginine to ornithine—were higher in preeclamptic villi than in normotensive pregnancy. These results provide a biochemical explanation for defective NO activity and increased oxidative stress in preeclamptic placenta. In normal placenta, adequate concentration of l-arginine orients ecNOS toward NO. In preeclampsia, a lower than normal l-arginine concentration caused by arginase II overexpression redirects ecNOS toward peroxynitrite.
Coronary Kinin Generation Mediates Nitric Oxide Release After Angiotensin Receptor Stimulation
- Nahid Seyedi,
- XiaoBin Xu,
- Alberto Nasjletti and
- Thomas H. Hintze
Hypertension Volume 26, Issue 11 July 1995

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Abstract Our goal was to determine whether angiotensin II (Ang II) and its metabolic fragments release nitric oxide and the mechanisms by which this occurs in blood vessels from the canine heart. We incubated 20 mg of microvessels or large coronary arteries in phosphate-buffered saline for 20 minutes and measured nitrite release. Nitrite release increased from 27±2 up to 103±5, 145±17, 84±4, 107±16, and 54±4 pmol/mg (P<.05) in response to 10⁻⁵ mol/L of Ang I, II, III, IV, and Ang-(1-7), respectively. The effects of all angiotensins were blocked by N^ω-nitro-l-arginine methyl ester (100 μmol/L), indicating that nitrite was a product of nitric oxide metabolism, and by Hoe 140 (10 μmol/L), a specific bradykinin B₂ receptor antagonist, indicating a potential role for local kinin formation. The protease inhibitors aprotinin (10 μmol/L) and soybean trypsin inhibitor, which block local kinin formation, inhibited nitrite release by all of the angiotensins. Angiotensin nonselective (saralasin), type 1–specific (losartan), and type 2–specific (PD 123319) receptor antagonists abolished the nitrite released in response to all the fragments. Angiotensin type 1 and type 2 and receptors mediate nitrite release after Ang I, II, III, and Ang-(1-7), whereas only type 2 receptors mediate nitrite release after Ang IV. Similar results were obtained in large coronary arteries. In summary, formation of nitrite from coronary microvessels and large arteries in the normal dog heart in response to angiotensin peptides is due to the activation of local kinin production in the coronary vessel wall.
Endothelin-1 Inhibits Nitric Oxide Synthesis in Vascular Smooth Muscle Cells
- Uichi Ikeda,
- Keiji Yamamoto,
- Yoshikazu Maeda,
- Masahisa Shimpo,
- Toshiko Kanbe and
- Kazuyuki Shimada
Hypertension Volume 29, Issue 11 January 1997

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We investigated the effects of endothelin-1 on nitric oxide synthesis in vascular smooth muscle cells. We measured the production of nitrite, a stable metabolite of nitric oxide, and the expression of inducible nitric oxide synthase mRNA and protein in cultured rat vascular smooth muscle cells. Incubation of the cultures with interleukin-1β (10 ng/mL) for 24 hours caused a significant increase in nitrite production. Endothelin-1 significantly decreased the interleukin-1β–induced nitrite production by vascular smooth muscle cells in a dose-dependent manner (10⁻¹¹ to 10⁻⁸ mol/L). Incubation with interleukin-1β for 24 hours induced expression of inducible nitric oxide synthase mRNA and protein in vascular smooth muscle cells, whereas endothelin-1 showed a suppressive effect on their expressions. Addition of the endothelin type A receptor antagonist BQ-485, but not the endothelin type B receptor antagonist BQ-788, dose-dependently inhibited the effect of endothelin-1. After protein kinase C activity was functionally depleted by treatment of cells with phorbol 12-myristate 13-acetate for 24 hours, the effect of endothelin-1 was abolished. These results indicate that endothelin-1 acts on endothelin type A receptors and inhibits nitric oxide synthesis in interleukin-1β–stimulated vascular smooth muscle cells at least partially through a protein kinase C–dependent pathway.
Subpressor Dose of L-NAME Unmasks Hypertensive Effect of Chronic Hyperinsulinemia
- Michael Bursztyn,
- Judith Mekler,
- Edna Peleg and
- Jacques Bernheim
Hypertension Volume 36, Issue 51 November 2000

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Abstract—We previously found that chronic exogenous hyperinsulinemia without sugar supplementation does not elevate blood pressure. This may be partially explained by the ability of insulin to release nitric oxide and cause vasodilatation. To test this hypothesis, we studied 4 groups of rats: 9 rats (body weight, 213±14 g) treated with a gradual increase of a sustained-release subcutaneous insulin pellet; 9 rats (body weight, 213±9 g) treated with N^G-nitro-l-arginine methyl ester (L-NAME) in drinking water 50 mg/L; 19 rats (body weight, 217±11 g) treated with the combination of L-NAME and insulin; and 9 control rats (body weight, 218±11 g). Blood pressure was followed weekly for 6 weeks, and then rats were studied in metabolic cages. Weight gain was not different during the 6 weeks. Renal function did not differ between the 4 groups, but 24-hour urinary nitrite/nitrate excretion was lower (P<0.02) in L-NAME–treated and higher in insulin-treated rats. Plasma insulin doubled (P<0.002) in the insulin-treated rats, but there was no hypoglycemia and, by week 6, fructosamine levels were 2.1±0.2, 2.1±0.2, 2.3±0.1, and 2.3±0.2 mmol/L in control rats and rats treated with L-NAME, insulin, and L-NAME plus insulin, respectively. Systolic blood pressure, which did not differ at baseline, at week 3 was 122±17, 118±17, and 118±24 mm Hg in the control, L-NAME, and insulin groups and 136±14 mm Hg (P<0.03) in the combination group. At week 6, systolic blood pressure was 128±14, 127±15, and 118±13 mm Hg in the control, L-NAME, and insulin groups, respectively, and 150±14 mm Hg (P<0.0005) in the combination group. In a subsequent experiment, l-arginine 2 g/L abrogated the effects of L-NAME and insulin combination. In conclusion, chronic exogenous hyperinsulinemia does not affect blood pressure but may cause hypertension when endothelial function is compromised.
Is Nitrite the Circulating Endocrine Effector of Remote Ischemic Preconditioning?
- Paola Corti and
- Mark T. Gladwin
Circulation Research Volume 114, Issue 109 May 2014

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Hypoxic Modulation of Exogenous Nitrite-Induced Vasodilation in Humans
- Abdul R. Maher,
- Alexandra B. Milsom,
- Prasad Gunaruwan,
- Khalid Abozguia,
- Ibrar Ahmed,
- Rebekah A. Weaver,
- Philip Thomas,
- Houman Ashrafian,
- Gustav V.R. Born,
- Philip E. James and
- Michael P. Frenneaux
Circulation Volume 117, Issue 55 February 2008

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Background— It has been proposed that under hypoxic conditions, nitrite may release nitric oxide, which causes potent vasodilation. We hypothesized that nitrite would have a greater dilator effect in capacitance than in resistance vessels because of lower oxygen tension and that resistance-vessel dilation should become more pronounced during hypoxemia. The effect of intra-arterial infusion of nitrite on forearm blood flow and forearm venous volumes was assessed during normoxia and hypoxia.Methods and Results— Forty healthy volunteers were studied. After baseline infusion of 0.9% saline, sodium nitrite was infused at incremental doses from 40 nmol/min to 7.84 μmol/min. At each stage, forearm blood flow was measured by strain-gauge plethysmography. Forearm venous volume was assessed by radionuclide plethysmography. Changes in forearm blood flow and forearm venous volume in the infused arm were corrected for those in the control arm. The peak percentage of venodilation during normoxia was 35.8±3.4% (mean±SEM) at 7.84 μmol/min (P<0.001) and was similar during hypoxia. In normoxia, arterial blood flow, assessed by the forearm blood flow ratio, increased from 1.04±0.09 (baseline) to 1.62±0.18 (nitrite; P<0.05) versus 1.07±0.09 (baseline) to 2.37±0.15 (nitrite; P<0.005) during hypoxia. This result was recapitulated in vitro in vascular rings.Conclusions— Nitrite is a potent venodilator in normoxia and hypoxia. Arteries are modestly affected in normoxia but potently dilated in hypoxia, which suggests the important phenomenon of hypoxic augmentation of nitrite-mediated vasodilation in vivo. The use of nitrite as a selective arterial vasodilator in ischemic territories and as a potent venodilator in heart failure has therapeutic implications.
Dietary Nitrate Supplementation Improves Revascularization in Chronic Ischemia
- Ulrike B. Hendgen-Cotta,
- Peter Luedike,
- Matthias Totzeck,
- Martina Kropp,
- Andreas Schicho,
- Pia Stock,
- Christos Rammos,
- Michael Niessen,
- Christian Heiss,
- Jon O. Lundberg,
- Eddie Weitzberg,
- Malte Kelm and
- Tienush Rassaf
Circulation Volume 126, Issue 1616 October 2012

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Background—Revascularization is an adaptive repair mechanism that restores blood flow to undersupplied ischemic tissue. Nitric oxide plays an important role in this process. Whether dietary nitrate, serially reduced to nitrite by commensal bacteria in the oral cavity and subsequently to nitric oxide and other nitrogen oxides, enhances ischemia-induced remodeling of the vascular network is not known.Methods and Results—Mice were treated with either nitrate (1 g/L sodium nitrate in drinking water) or sodium chloride (control) for 14 days. At day 7, unilateral hind-limb surgery with excision of the left femoral artery was conducted. Blood flow was determined by laser Doppler. Capillary density, myoblast apoptosis, mobilization of CD34⁺/Flk-1⁺, migration of bone marrow–derived CD31⁺/CD45⁻, plasma S-nitrosothiols, nitrite, and skeletal tissue cGMP levels were assessed. Enhanced green fluorescence protein transgenic mice were used for bone marrow transplantation. Dietary nitrate increased plasma S-nitrosothiols and nitrite, enhanced revascularization, increased mobilization of CD34⁺/Flk-1⁺ and migration of bone marrow–derived CD31⁺/CD45⁻ cells to the site of ischemia, and attenuated apoptosis of potentially regenerative myoblasts in chronically ischemic tissue. The regenerative effects of nitrate treatment were abolished by eradication of the nitrate-reducing bacteria in the oral cavity through the use of an antiseptic mouthwash.Conclusions—Long-term dietary nitrate supplementation may represent a novel nutrition-based strategy to enhance ischemia-induced revascularization.
Paradoxical Normoxia-Dependent Selective Actions of Inorganic Nitrite in Human Muscular Conduit Arteries and Related Selective Actions on Central Blood Pressures
- Sami A. Omar,
- Henry Fok,
- Katharina D. Tilgner,
- Ashok Nair,
- Joanne Hunt,
- Benyu Jiang,
- Paul Taylor,
- Phil Chowienczyk and
- Andrew J. Webb
Circulation Volume 131, Issue 427 January 2015

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Background—Inorganic nitrite dilates small resistance arterioles via hypoxia-facilitated reduction to vasodilating nitric oxide. The effects of nitrite in human conduit arteries have not been investigated. In contrast to nitrite, organic nitrates are established selective dilators of conduit arteries.Methods and Results—We examined the effects of local and systemic administration of sodium nitrite on the radial artery (a muscular conduit artery), forearm resistance vessels (forearm blood flow), and systemic hemodynamics in healthy male volunteers (n=43). Intrabrachial sodium nitrite (8.7 μmol/min) increased radial artery diameter by a median of 28.0% (25th and 75th percentiles, 25.7% and 40.1%; P<0.001). Nitrite (0.087–87 μmol/min) displayed conduit artery selectivity similar to that of glyceryl trinitrate (0.013–4.4 nmol/min) over resistance arterioles. Nitrite dose-dependently increased local cGMP production at the dose of 2.6 μmol/min by 1.1 pmol·min⁻¹·100 mL⁻¹ tissue (95% confidence interval, 0.5–1.8). Nitrite-induced radial artery dilation was enhanced by administration of acetazolamide (oral or intra-arterial) and oral raloxifene (P=0.0248, P<0.0001, and P=0.0006, respectively) but was inhibited under hypoxia (P<0.0001) and hyperoxia (P=0.0006) compared with normoxia. Systemic intravenous administration of sodium nitrite (8.7 μmol/min) dilated the radial artery by 10.7% (95% confidence interval, 6.8–14.7) and reduced central systolic blood pressure by 11.6 mm Hg (95% confidence interval, 2.4–20.7), augmentation index, and pulse wave velocity without changing peripheral blood pressure.Conclusions—Nitrite selectively dilates conduit arteries at supraphysiological and near-physiological concentrations via a normoxia-dependent mechanism that is associated with cGMP production and is enhanced by acetazolamide and raloxifene. The selective central blood pressure–lowering effects of nitrite have therapeutic potential to reduce cardiovascular events.
Can Nitrite AMP_k Up Sirt-ainty to Treat Heart Failure With Preserved Ejection Fraction?
- Steven Hsu and
- David A. Kass
Circulation Volume 133, Issue 823 February 2016

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Dietary Nitrate Provides Sustained Blood Pressure Lowering in Hypertensive Patients: A Randomized, Phase 2, Double-Blind, Placebo-Controlled Study
- Vikas Kapil,
- Rayomand S. Khambata,
- Amy Robertson,
- Mark J. Caulfield and
- Amrita Ahluwalia
Hypertension Volume 65, Issue 21 February 2015

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Abstract—Single dose administration of dietary inorganic nitrate acutely reduces blood pressure (BP) in normotensive healthy volunteers, via bioconversion to the vasodilator nitric oxide. We assessed whether dietary nitrate might provide sustained BP lowering in patients with hypertension. We randomly assigned 68 patients with hypertension in a double-blind, placebo-controlled clinical trial to receive daily dietary supplementation for 4 weeks with either dietary nitrate (250 mL daily, as beetroot juice) or a placebo (250 mL daily, as nitrate-free beetroot juice) after a 2-week run-in period and followed by a 2-week washout. We performed stratified randomization of drug-naive (n=34) and treated (n=34) patients with hypertension aged 18 to 85 years. The primary end point was change in clinic, ambulatory, and home BP compared with placebo. Daily supplementation with dietary nitrate was associated with reduction in BP measured by 3 different methods. Mean (95% confidence interval) reduction in clinic BP was 7.7/2.4 mm Hg (3.6–11.8/0.0–4.9, P<0.001 and P=0.050). Twenty-four-hour ambulatory BP was reduced by 7.7/5.2 mm Hg (4.1–11.2/2.7–7.7, P<0.001 for both). Home BP was reduced by 8.1/3.8 mm Hg (3.8–12.4/0.7–6.9, P<0.001 and P<0.01) with no evidence of tachyphylaxis over the 4-week intervention period. Endothelial function improved by ≈20% (P<0.001), and arterial stiffness was reduced by 0.59 m/s (0.24–0.93; P<0.01) after dietary nitrate consumption with no change after placebo. The intervention was well tolerated. This is the first evidence of durable BP reduction with dietary nitrate supplementation in a relevant patient group. These findings suggest a role for dietary nitrate as an affordable, readily-available, adjunctive treatment in the management of patients with hypertension (funded by The British Heart Foundation).Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01405898.
Vasorelaxation to the Nitroxyl Donor Isopropylamine NONOate in Resistance Arteries Does Not Require Perivascular Calcitonin Gene–Related Peptide
Hypertension Volume 70, Issue 31 September 2017

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Nitroxyl (HNO) donors offer considerable therapeutic potential for the treatment of hypertension-related cardiovascular disorders, particularly heart failure, as they combine an inotropic action with peripheral vasodilation. Angeli’s salt is the only HNO donor whose mechanism has been studied in depth, and recently, Angeli’s salt vasodilation was suggested to be indirect and caused by calcitonin gene–related peptide (CGRP) released from perivascular nerves after HNO activates TRPA1 (transient receptor potential cation channel subfamily A member 1) channels. We investigated resistance artery vasorelaxation to the HNO donor, isopropylamine NONOate (IPA/NO), one of the structures providing a template for therapeutic development. Wire myography in combination with measurements of smooth muscle membrane potential was used to characterize the effect of IPA/NO in mesenteric resistance arteries. Immunohistochemistry was assessed in pressurized arteries. IPA/NO concentration dependently hyperpolarized and relaxed arteries precontracted with the α₁-adrenoreceptor agonist, phenylephrine. These effects were blocked by the soluble guanylyl cyclase inhibitor, ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) but not by the K_ATP channel inhibitor, glibenclamide. Vasorelaxation persisted in the presence of raised [K⁺]_o, used to block hyperpolarization, capsaicin to deplete perivascular CGRP, or HC030031 (2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4 isopropylphenyl) acetamide) to block TRPA1 receptors. Without preconstriction, hyperpolarization to IPA/NO was suppressed by glibenclamide, capsaicin, or HC030031. Hyperpolarization but not vasorelaxation to exogenous CGRP was inhibited with glibenclamide. Thus, vascular hyperpolarization is not necessary for vasorelaxation to the HNO donor IPA/NO, even though both effects are cGMP dependent. The reduced hyperpolarization after depletion of perivascular CGRP or block of TRPA1 receptors indicates some release of CGRP, but this does not contribute to HNO vasorelaxation. Therefore, HNO–TRPA1–CGRP signaling does not seem important for vasodilation to IPA/NO in resistance arteries.
Altered Oral Nitrate Reduction and Bacterial Profiles in Hypertensive Women Predict Blood Pressure Lowering Following Acute Dietary Nitrate Supplementation
- Thomas Willmott,
- Laura Ormesher,
- Andrew J. McBain,
- Gavin J. Humphreys,
- Jenny E. Myers,
- Gurdeep Singh,
- Jon O. Lundberg,
- Eddie Weitzberg,
- Carina Nihlen and
- Elizabeth C. Cottrell
Hypertension Volume 80, Issue 111 November 2023

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BACKGROUND:The efficacy of dietary nitrate supplementation to lower blood pressure (BP) in pregnant women is highly variable. We aimed to investigate whether differences in oral microbiota profiles and oral nitrate-reducing capacity may explain interindividual differences in BP lowering following nitrate supplementation.METHODS:Participants recruited for this study were both pregnant and nonpregnant women, with or without hypertension (n=55). Following an overnight fast, plasma, saliva, and tongue scraping samples were collected for measurement of nitrate/nitrite concentrations, oral NaR (nitrate reductase) activity, and microbiota profiling using 16S rRNA gene sequencing. Baseline BP was measured, followed by the administration of a single dose of dietary nitrate (400 mg nitrate in 70 mL beetroot juice). Post-nitrate intervention, plasma and salivary nitrate/nitrite concentrations and BP were determined 2.5 hours later.RESULTS:Women with hypertension had significantly lower salivary nitrite concentrations (P=0.006) and reduced abundance of the nitrate-reducing taxa Veillonella(P=0.007) compared with normotensive women. Oral NaR activity was not significantly different in pregnant versus nonpregnant women (P=0.991) but tended to be lower in hypertensive compared with normotensive women (P=0.099). Oral NaR activity was associated with both baseline diastolic BP (P=0.050) and change in diastolic BP following acute nitrate intake (P=0.01, adjusted for baseline BP).CONCLUSIONS:The abundance and activity of oral nitrate-reducing bacteria impact both baseline BP as well as the ability of dietary nitrate supplementation to lower BP. Strategies to increase oral nitrate-reducing capacity could lower BP and enhance the efficacy of dietary nitrate supplementation, in pregnancy as well as in nonpregnant adults.REGISTRATION:URL: https://www.clinicaltrials.gov; Unique identifier: NCT03930693.Graphical Abstract
Nitrites, Nitrates, and Cardiovascular Outcomes: Are We Living “La Vie en Rose” With Pink Processed Meats?
- Bernard Srour,
- Eloi Chazelas,
- Léopold K. Fezeu,
- Guillaume Javaux,
- Fabrice Pierre,
- Inge Huybrechts,
- Serge Hercberg,
- Mélanie Deschasaux‐Tanguy,
- Emmanuelle Kesse‐Guyot and
- Mathilde Touvier
Journal of the American Heart Association Volume 11, Issue 2420 December 2022

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BackgroundNitrates and nitrites are used as food additives in processed meats. They are also commonly ingested from water and several foods. Several short‐term clinical studies suggested beneficial effects of dietary nitrates on blood pressure, while deleterious effects on oxidative damage have been suggested in some experimental studies. However, there is a lack of evidence from longitudinal epidemiological studies linking foods and water‐originated and additives‐originated nitrites and nitrates, separately, to hypertension and cardiovascular diseases risk. We aimed to study these associations in a large population‐based cohort.Methods and ResultsOverall, 106 288 adults from the French NutriNet‐Santé cohort (2009–2022) were included. Associations between nitrites and nitrates intakes and hypertension and cardiovascular disease risks were assessed using multi‐adjusted Cox proportional hazard models. During follow‐up, 3810 incident cases of hypertension and 2075 cases of cardiovascular diseases were ascertained. Participants with higher intakes of additives‐originated nitrites (sodium nitrite in particular [European code e250]) had a higher hypertension risk compared with nonconsumers (hazard ratio, 1.19 [95% CI, 1.08–1.32], P=0.001, and 1.19 [95% CI, 1.08–1.32], P=0.002), respectively. No association was detected between foods and water‐originated nitrites, or nitrates with hypertension risk (all P values >0.3). We found no association between nitrites or nitrates and risks of cardiovascular diseases (all P values >0.2).ConclusionsThese results do not support a protective role of nitrites or nitrates in cardiovascular health. Instead, they suggest a positive association between nitrites from food additives and hypertension risk, which needs confirmation in other large‐scale studies. These findings provide new evidence in the context of current discussions about updating regulations on the use of nitrites as food additives.

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l-Arginine Depletion in Preeclampsia Orients Nitric Oxide Synthase Toward Oxidant Species

Abstract

Coronary Kinin Generation Mediates Nitric Oxide Release After Angiotensin Receptor Stimulation

Abstract

Endothelin-1 Inhibits Nitric Oxide Synthesis in Vascular Smooth Muscle Cells

Abstract

Subpressor Dose of L-NAME Unmasks Hypertensive Effect of Chronic Hyperinsulinemia

Abstract

Is Nitrite the Circulating Endocrine Effector of Remote Ischemic Preconditioning?

Abstract

Hypoxic Modulation of Exogenous Nitrite-Induced Vasodilation in Humans

Abstract

Dietary Nitrate Supplementation Improves Revascularization in Chronic Ischemia

Abstract

Paradoxical Normoxia-Dependent Selective Actions of Inorganic Nitrite in Human Muscular Conduit Arteries and Related Selective Actions on Central Blood Pressures

Abstract

Can Nitrite AMP_k Up Sirt-ainty to Treat Heart Failure With Preserved Ejection Fraction?

Abstract

Dietary Nitrate Provides Sustained Blood Pressure Lowering in Hypertensive Patients: A Randomized, Phase 2, Double-Blind, Placebo-Controlled Study

Abstract

Vasorelaxation to the Nitroxyl Donor Isopropylamine NONOate in Resistance Arteries Does Not Require Perivascular Calcitonin Gene–Related Peptide

Abstract

Altered Oral Nitrate Reduction and Bacterial Profiles in Hypertensive Women Predict Blood Pressure Lowering Following Acute Dietary Nitrate Supplementation

Abstract

Nitrites, Nitrates, and Cardiovascular Outcomes: Are We Living “La Vie en Rose” With Pink Processed Meats?

Abstract