Long-term nitric oxide blockade in the pregnant rat: Effects on blood pressure and plasma levels of endothelin-1

Background. Pregnancy-induced hypertension (PIH) remains a major cause of morbidity and mortality in pregnancy worldwide. This study was designed to study the blood pressure-lowering effect of resveratrol (RES) in a salt-induced hypertensive pregnant rat model. Methods. Forty female Sprague Dawley (SD) rats were randomized into 4 groups: Normal Preg (0.9% salt diet), Normal Preg + RES (0.9% salt diet plus daily oral RES for 4 weeks), Salt Preg (8% salt diet), and Salt Preg + RES (8% salt diet plus daily oral RES for 4 weeks). Noninvasive blood pressure was recorded on gestational days 7 and 14. On the gestational day 19, foetuses were weighed, and blood and urine samples were harvested for electrolytes and biochemical assays. Results. RES significantly reduced SBP, DBP, and MAP on gestational days 7 and 14 in the Salt Preg + RES group compared to the Salt Preg group (all P<0.05). Compared to the Salt Preg group, the foetal weight, serum NO level, urinary sodium, and 24 hour urine volume were significantly increased in the Salt Preg + RES group (all P<0.05). On the contrary, the levels of serum urea, serum creatinine, and urinary protein were significantly decreased in the Salt Preg + RES group compared to the Salt Preg group (all P<0.05). Conclusions. RES decreases blood pressure in a hypertensive pregnant rat model. Increasing sodium excretion and serum nitric oxide level might be, at least part of, the underlying mechanisms.

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Physiological persona differences based on stress and inflammation between meditators and healthy controls

Journal of Complementary and Integrative Medicine ◽

10.1515/jcim-2019-0106 ◽

2019 ◽

Vol 17 (2) ◽

Cited By ~ 1

Author(s):

Dipti Magan ◽

Raj Kumar Yadav

Keyword(s):

Blood Pressure ◽

Body Mass Index ◽

Plasma Levels ◽

Inflammatory Markers ◽

Tumor Necrosis ◽

Healthy Controls ◽

Short Term ◽

Tnf Α ◽

Necrosis Factor

AbstractBackgroundNowadays, yoga is endorsed and advised routinely to stay fit and healthy, as well as control many chronic diseases including diabetes type 2, hypertension, coronary artery diseases, etc. Now, our assumption is that those who do regular yoga have different persona than who do not do yoga regularly. We planned to test our hypothesis scientifically, and therefore baseline physiological characteristics with stress and inflammation levels in long-term and short-term meditators and healthy novice controls were analyzed.MethodsIn this retrospective analysis, 97 male participants were included for their Baseline analysis. Fifteen apparently healthy subjects practicing preksha meditation (since >5 years, at least 5 days a week) were included as long-term meditators (LTMs); 58 subjects who attended one of our short-term yoga-based lifestyle intervention programs for 2 weeks were included as short-term meditators (STMs); 24 male novice subjects, who did not participate in any yogic intervention, were included as healthy controls. Here, we analyzed the Baseline plasma levels of stress and inflammatory markers, cortisol, β-endorphin, interleukin (IL)-6 and tumor necrosis factor (TNF)-α in long-term meditators vs. short-term meditators vs. healthy controls.Outcome measuresThe study parameters body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), plasma levels of stress and immune markers, cortisol, β-endorphin (β-Ed), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), were assessed in all the three groups at baseline.ResultsSignificant (p<0.05) differences were observed at baseline for plasma levels of stress and inflammatory markers as well as body mass index and systolic blood pressure among LTM vs. STM vs. healthy controls.ConclusionsOur observations suggest that the subjects who do regular yoga-meditation practice have better stress & inflammation status than comparable age matched healthy controls.

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Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.90506.2008 ◽

2009 ◽

Vol 296 (2) ◽

pp. R195-R200 ◽

Cited By ~ 67

Author(s):

Dan Wang ◽

Svend Strandgaard ◽

Jens Iversen ◽

Christopher S. Wilcox

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Blood Pressure ◽

Essential Hypertension ◽

Nitric Oxide Synthase ◽

Plasma Levels ◽

Asymmetric Dimethylarginine ◽

Lipid Peroxidation Product ◽

Individual Values ◽

Oxide Synthase

We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension ( n = 9) compared with normal controls ( n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric dimethylarginine (ADMA), or the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid (HODE), which is a marker of reactive oxygen species. Patients had significantly ( P < 0.001) elevated (means ± SD) plasma levels of ADMA (PADMA, 766 ± 217 vs. 393 ± 57 nmol/l) and symmetric dimethylarginine (PSDMA: 644 ± 140 vs. 399 ± 70 nmol/l) but similar levels of l-arginine accompanied by significantly ( P < 0.015) increased rates of renal ADMA excretion (21 ± 9 vs. 14 ± 5 nmol/μmol creatinine) and decreased rates of renal ADMA clearance (18 ± 3 vs. 28 ± 5 ml/min). They had significantly increased plasma levels of HODE (PHODE: 309 ± 30 vs. 226 ± 24 nmol/l) and renal HODE excretion (433 ± 93 vs. 299 ± 67 nmol/μmol creatinine). For the combined group of normal and hypertensive subjects, the individual values for plasma levels of ADMA and HODE were both significantly ( P < 0.001) and inversely correlated with microvascular EDRF/NO and positively correlated with mean blood pressure. In conclusion, elevated levels of ADMA and oxidative stress in a group of hypertensive patients could contribute to the associated microvascular endothelial dysfunction and elevated blood pressure.

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Chronic Blockade of Neuronal Nitric Oxide Synthase Does Not Affect Long-Term Control of Blood Pressure in Normal, Saline-Drinking or Deoxycorticosterone-Treated Rats

Experimental Physiology ◽

10.1113/eph8802489 ◽

2003 ◽

Vol 88 (2) ◽

pp. 243-250 ◽

Cited By ~ 10

Author(s):

Rosemary Wangensteen ◽

Juan Sainz ◽

Isabel Rodríguez-Gomez ◽

Juan Manuel Moreno ◽

Antonio Osuna ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Nitric Oxide Synthase ◽

Normal Saline ◽

Neuronal Nitric Oxide Synthase ◽

Oxide Synthase

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EFFECTS OF ANTIHYPERTENSIVE DRUGS ON PLASMA LEVELS OF NITRIC OXIDE DERIVATES PRODUCTS AND ASYMMETRIC DIMETHYLARGININE IN TARGET ACHIEVED SYSTOLIC BLOOD PRESSURE PATIENTS: PP.6.263

Journal of Hypertension ◽

10.1097/01.hjh.0000378587.92774.94 ◽

2010 ◽

Vol 28 ◽

pp. e128

Author(s):

A Galyavich ◽

A Khamidullina ◽

R Galyavi

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Systolic Blood Pressure ◽

Plasma Levels ◽

Asymmetric Dimethylarginine ◽

Antihypertensive Drugs

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Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1

Endocrinology ◽

10.1210/en.2008-1360 ◽

2009 ◽

Vol 150 (5) ◽

pp. 2382-2387 ◽

Cited By ~ 11

Author(s):

Karim Sabrane ◽

Markus-N. Kruse ◽

Alexandra Gazinski ◽

Michaela Kuhn

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Methyl Ester ◽

Atrial Natriuretic Peptide ◽

Arterial Blood Pressure ◽

Natriuretic Peptide ◽

Endothelin 1 ◽

Arterial Blood ◽

Atrial Natriuretic

Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.

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