scholarly journals Blood Pressure Regulation in Stress: Focus on Nitric Oxide-Dependent Mechanisms

2016 ◽  
pp. S309-S342 ◽  
Author(s):  
A. PUZSEROVA ◽  
I. BERNATOVA
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Vascular Function ◽  
Malignant Tumors ◽  
Current Knowledge ◽  
Cardiovascular Responses ◽  
Special Focus ◽  
Induced Hypertension ◽  
Neuroendocrine Mechanisms ◽  
No Bioavailability

Stress is considered a risk factor associated with the development of various civilization diseases including cardiovascular diseases, malignant tumors and mental disorders. Research investigating mechanisms involved in stress-induced hypertension have attracted much attention of physicians and researchers, however, there are still ambiguous results concerning a causal relationship between stress and long-term elevation of blood pressure (BP). Several studies have observed that mechanisms involved in the development of stress-induced hypertension include increased activity of sympathetic nervous system (SNS), glucocorticoid (GC) overload and altered endothelial function including decreased nitric oxide (NO) bioavailability. Nitric oxide is well known neurotransmitter, neuromodulator and vasodilator involved in regulation of neuroendocrine mechanisms and cardiovascular responses to stressors. Thus NO plays a crucial role in the regulation of the stress systems and thereby in the BP regulation in stress. Elevated NO synthesis, especially in the initial phase of stress, may be considered a stress-limiting mechanism, facilitating the recovery from stress to the resting levels via attenuation of both GC release and SNS activity as well as by increased NO-dependent vasorelaxation. On the other hand, reduced levels of NO were observed in the later phases of stress and in subjects with genetic predisposition to hypertension, irrespectively, in which reduced NO bioavailability may account for disruption of NO-mediated BP regulatory mechanisms and accentuated SNS and GC effects. This review summarizes current knowledge on the role of stress in development of hypertension with a special focus on the interactions among NO and other biological systems affecting blood pressure and vascular function.

Cardiovascular Responses to Muscle Stretching: A Systematic Review and Meta-analysis

2021 ◽  
Author(s):  
Ewan Thomas ◽  
Marianna Bellafiore ◽  
Ambra Gentile ◽  
Antonio Paoli ◽  
Antonio Palma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular System ◽  
Vascular Function ◽  
Meta Analysis ◽  
Random Effect ◽  
Cardiovascular Responses ◽  
Qualitative Description ◽  
Cross Sectional ◽  
Quantitative Synthesis

AbstractThe aim of this study will be to review the current body of literature to understand the effects of stretching on the responses of the cardiovascular system. A literature search was performed using the following databases: Scopus, NLM Pubmed and ScienceDirect. Studies regarding the effects of stretching on responses of the cardiovascular system were investigated. Outcomes regarded heart rate(HR), blood pressure, pulse wave velocity (PWV of which baPWV for brachial-ankle and cfPWV for carotid-femoral waveforms), heart rate variability and endothelial vascular function. Subsequently, the effects of each outcome were quantitatively synthetized using meta-analytic synthesis with random-effect models. A total of 16 studies were considered eligible and included in the quantitative synthesis. Groups were also stratified according to cross-sectional or longitudinal stretching interventions. Quality assessment through the NHLBI tools observed a “fair-to-good” quality of the studies. The meta-analytic synthesis showed a significant effect of d=0.38 concerning HR, d=2.04 regarding baPWV and d=0.46 for cfPWV. Stretching significantly reduces arterial stiffness and HR. The qualitative description of the studies was also supported by the meta-analytic synthesis. No adverse effects were reported, after stretching, in patients affected by cardiovascular disease on blood pressure. There is a lack of studies regarding vascular adaptations to stretching.

Effect of magnesium supplementation on blood pressure and vascular reactivity in nitric oxide synthase inhibition-induced hypertension model

2015 ◽  
Vol 37 (8) ◽  
pp. 633-642 ◽  
Author(s):  
Filiz Basralı ◽  
Günnur Koçer ◽  
Pınar Ülker Karadamar ◽  
Seher Nasırcılar Ülker ◽  
Leyla Satı ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Magnesium Supplementation ◽  
Induced Hypertension ◽  
Oxide Synthase

Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in normotensive rats

2001 ◽  
Vol 281 (2) ◽  
pp. H975-H980 ◽  
Author(s):  
Hui Xu ◽  
Gregory D. Fink ◽  
Alex Chen ◽  
Stephanie Watts ◽  
James J. Galligan
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Nerve Activity ◽  
Nitric Oxide Synthase Inhibitor ◽  
Arterial Blood ◽  
Independent Effects ◽  
Synthase Inhibitor

The role of the sympathetic nervous system in 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (tempol)-induced cardiovascular responses in urethane-anesthetized, normotensive rats was evaluated. Tempol caused dose-dependent (30–300 μmol/kg iv) decreases in renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MAP), and heart rate (HR). Similar responses were obtained after sinoaortic denervation and cervical vagotomy. These responses were not blocked following treatment with the nitric oxide synthase inhibitor N G-nitro-l-arginine (2.6 mg · kg−1 · min−1 iv for 5 min) or the α2-adrenergic receptor antagonist idazoxan (0.3 mg/kg iv bolus). Idazoxan blocked the effects of clonidine (10 μg/kg iv) on HR, MAP, and RSNA. Hexamethonium (30 mg/kg iv) inhibited RSNA, and tempol did not decrease RSNA after hexamethonium. The effects of tempol on HR and MAP were reduced by hexamethonium. In conclusion, depressor responses caused by tempol are mediated, partly, by sympathoinhibition in urethane-anesthetized, normotensive rats. Nitric oxide does not contribute to this response, and the sympathoinhibitory effect of tempol is not mediated via α2-adrenergic receptors. Finally, tempol directly decreases HR, which may contribute to the MAP decrease.

Clinical evaluation of nitric oxide responses to anti-VEGF therapy with bevacizumab

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14039-14039 ◽  
Author(s):  
A. Nixon ◽  
J. Allen ◽  
E. Miller ◽  
S. Savage ◽  
N. Kaplan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Brachial Artery ◽  
Exhaled No ◽  
Anti Vegf ◽  
Signed Rank ◽  
Post Infusion ◽  
No Bioavailability ◽  
Pre Treatment ◽  
Hyperemic Flow

14039 Background: Anti-vascular endothelial growth factor (anti-VEGF) therapy has been linked to hypertension (HTN) and arterial thrombo-embolic events that may involve changes in nitric oxide (NO) bioavailability. Methods: 25 patients (pts) with advanced cancer, normal renal function and blood pressure (BP), no increased risks for anti-VEGF toxicities, and not on medications known to confound biomarker studies (including anti-hypertensives) were treated with bevacizumab (BV) 15mg/kg d1, then 10mg/kg q2 week. Prior to biomarker assessment, all patients were placed on a calorie-, nitrate-, and salt-restricted diet for 72 hr. All measures were taken pre-treatment (preRx) and on day 28 of treatment (onRx). Dependant variables included; a) Brachial artery reactivity (BAR) following hyperemic flow stimulus (endothelium-dependent) and sub-lingual nitroglycerine (NTG; endothelium-independent); b) exhaled and plasma/urine total NO2/NO3 using chemiluminescence (Sievers 280NOA) with either KI or VCl3 in HCl as the reductants; c) blood pressure. Additionally, we measured multiple regulators of vascular tone and injury. Comparisons were analyzed using Spearman signed rank tests. Results: Of 25 pts (16 F, 9 M) treated, 21 patients were fully evaluable. Significant changes or strong trends were observed upon comparing preRx vs. onRx for BP (SBP +12.4, DBP +5.6, MAP +7.9 mm Hg), and flow-mediated BAR (-2.0%) with no changes in hyperemic flow/shear stimulus or smooth muscle function (BAR NTG), indicating a decrease in brachial artery endothelial responsiveness. Exhaled NO decreased (-0.8% d1vs d28 and -0.6% pre/post infusion day1). Measurement and data analysis of urinary/plasma NO2/NO3, as well as angiogenic markers, are almost complete and will be reported. Conclusions: After one month of treatment, BV increased BP and decreased endothelium- dependent BAR and exhaled NO, suggesting potentially broad, mechanism-based effects on NO bioavailability in patients. [Table: see text]

scholarly journals The endocrine system in chronic nitric oxide deficiency

2007 ◽  
Vol 156 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Félix Vargas ◽  
Juan Manuel Moreno ◽  
Rosemary Wangensteen ◽  
Isabel Rodríguez-Gómez ◽  
Joaquín García-Estañ
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Pressure Response ◽  
Endocrine System ◽  
Special Focus ◽  
No Production ◽  
Regulatory Systems ◽  
Reported Study ◽  
Nitric Oxide Deficiency ◽  
Glucose And Lipid Homeostasis

The experimental model of chronic inhibition of nitric oxide (NO) production has proven to be a useful tool to study cardiovascular and renal lesions produced by this type of hypertension, which are similar to those found in human hypertension. It also offers a unique opportunity to study the interaction of NO with the humoral systems, known to have a role in the normal physiology of vascular tone and renal function. This review provides a thorough and updated analysis of the interactions of NO with the endocrine system. There is special focus on the main vasoactive factors, including the renin-angiotensin-aldosterone system, catecholamines, vasopressin, and endothelin among others. Recent discoveries of crosstalk between the endocrine system and NO are also reported. Study of these humoral interactions indicates that NO is a molecule with ubiquitous function and that its inhibition alters virtually to all other known regulatory systems. Thus, hypothyroidism attenuates the pressor effect of NO inhibitor N-nitro-L-arginine methyl ester, whereas hyperthyroidism aggravates the effects of NO synthesis inhibition; the sex hormone environment determines the blood pressure response to NO blockade; NO may play a homeostatic role against the prohypertensive effects of mineralocorticoids, thyroid hormones and insulin; and finally, NO deficiency affects not only blood pressure but also glucose and lipid homeostasis, mimicking the human metabolic syndrome X, suggesting that NO deficiency may be a link between metabolic and cardiovascular disease.

scholarly journals New Therapeutic Insight into the Effect of Ma Huang Tang on Blood Pressure and Renal Dysfunction in the L-NAME-Induced Hypertension

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Mi Hyeon Hong ◽  
Hye Yoom Kim ◽  
Youn Jae Jang ◽  
Se Won Na ◽  
Byung Hyuk Han ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Function ◽  
Intima Media Thickness ◽  
Dependent Manner ◽  
Vascular Relaxation ◽  
Sprague Dawley ◽  
Induced Hypertension ◽  
Ma Huang

In this study, we evaluated the effect of a traditional herbal formula, Ma Huang Tang (MHT), on blood pressure and vasodilation in a rat model of NG‐nitro‐L‐arginine methylester- (L-NAME-) induced hypertension. We found that MHT-induced vascular relaxation in a dose-dependent manner in rat aortas pretreated with phenylephrine. However, pretreatment of endothelium-intact aortic rings with L‐NAME, an inhibitor of nitric oxide synthesis (NOS), or 1H‐[1, 2, 4]‐oxadiazole‐[4, 3‐α]‐quinoxalin‐1‐one (ODQ), an inhibitor of soluble guanylyl cyclase, significantly abolished vascular relaxation induced by MHT. MHT also increased the production of guanosine 3′,5′-cyclic monophosphate (cGMP) in the aortic rings pretreated with L-NAME or ODQ. To examine the in vivo effects of MHT, Sprague Dawley rats were treated with 40 mg/kg/day L-NAME for 3 weeks, followed by administration of 50 or 100 mg/kg/day MHT for 2 weeks. MHT was found to significantly normalize systolic blood pressure and decreased intima-media thickness in aortic sections of rats treated with L-NAME compared to that of rats treated with L-NAME alone. MHT also restored the L-NAME-induced decrease in vasorelaxation response to acetylcholine and endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) expression. Furthermore, MHT promoted the recovery of renal function, as indicated by osmolality, blood urea nitrogen (BUN) levels, and creatinine clearance. These results suggest that MHT-induced relaxation in the thoracic aorta is associated with activation of the nitric oxide/cGMP pathway. Furthermore, it provides new therapeutic insights into the regulation of blood pressure and renal function in hypertensive patients.

scholarly journals Increase in Bioavailability of Nitric Oxide After Renal Denervation Improves Kidney Function in Sheep With Hypertensive Kidney Disease

Hypertension ◽  
2021 ◽  
Vol 77 (4) ◽  
pp. 1299-1310
Author(s):  
Reetu R. Singh ◽  
Zoe M. McArdle ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
Geoff A. Head ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Kidney Function ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Healthy Sheep ◽  
No Bioavailability

Overactivity of renal sympathetic nerves and nitric oxide (NO) deficiency occur in hypertensive chronic kidney disease (CKD). In sheep with hypertensive CKD and NO deficiency, renal denervation (RDN) reduces blood pressure and improves kidney function (glomerular filtration rate). We hypothesized that this improvement in glomerular filtration rate after RDN is associated with increased NO bioavailability. In this study, glomerular filtration rate response to systemic inhibition of NOS (NO synthase) was examined in healthy and CKD sheep at 2 and 30 months after a sham (intact nerves) or RDN procedure. Basal urinary total nitrate (nitrate+nitrite) excretion was examined at 2 and 30 months, and kidney protein expression of endothelial and neuronal NOS was assessed at 30 months. Urinary nitrate+nitrite in CKD-RDN and healthy sheep was ≈50% to 70% greater than in CKD-intact. During NOS inhibition, the fall in glomerular filtration rate in CKD-RDN sheep was ≈20% greater than in CKD-intact. These effects in CKD-RDN sheep were similar to those in healthy sheep. Endothelial NOS protein expression was lower in CKD-intact sheep compared with healthy sheep and compared with CKD-RDN. In summary, RDN normalizes NO bioavailability and restores contribution of NO to renal hemodynamics in CKD. These changes may promote improvements in kidney function and sustained blood pressure lowering after RDN in hypertensive CKD.

Abstract 4416: Genetic Variability of Methyl-Tetrahydrofolate-Reductase Modifies eNOS Coupling in Human Arteries and Veins: Effects on Vascular Superoxide Generation and Nitric Oxide Bioavailability

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Charalambos Antoniades ◽  
Cheerag Shrirodaria ◽  
Paul Leeson ◽  
Tim Van-Assche ◽  
Chanti Ratnatunga ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Function ◽  
Genotype Distribution ◽  
C677t Polymorphism ◽  
Mthfr Polymorphism ◽  
Vasomotor Responses ◽  
Mammary Arteries ◽  
Enos Uncoupling ◽  
No Bioavailability ◽  
Methyl Tetrahydrofolate

5-methyl-tetrahydrofolate (5MTHF) administration improves endothelial nitric oxide synthase (eNOS) coupling in human vessels. However, it is unclear whether endogenous variations of vascular 5MTHF levels due to the functional 5MTHF-reductase (MTHFR) polymorphism C677T, has an impact on vascular function. We examined the effect of this polymorphism on vascular 5MTHF levels, NO bioavailability and eNOS coupling in human vessels. The C677T polymorphism was determined in 218 patients undergoing coronary bypass surgery. Saphenous veins (SV) and internal mammary arteries (IMA) were obtained to determine vasomotor responses of SV to acetylcholine (ACh) ex-vivo, vascular O2- production (+/− eNOS inhibitor LNAME, by chemilumineschence) and vascular 5MTHF (by HPLC). The genotype distribution was CC:100(46%) CT:94(43%) and TT:24(11%). This polymorphism had a strong effect on vascular (Fig. a ) and plasma 5MTHF (p<0.001). Furthermore, the T allele was associated with lower vasomotor responses of SV to Ach (Fig. b ) as well as higher vascular O2- (Fig. c ) and greater LNAME inhibitable O2- (Fig d ., suggesting eNOS uncoupling) in IMA segments. The C677T polymorphism on MTHFR gene is a strong determinant of vascular 5MTHF, and has a significant effect on NO bioavailability and vascular redox state, by modifying eNOS coupling in human vessels.

Abstract 16884: Involvement of Hydrogen Sulfide (H2S) in Dexamethasone (DEX) Induced Hypertension in Rat

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Erminia Donnarumma ◽  
Emma Mitidieri ◽  
Teresa Tramontano ◽  
Vincenzo Brancaleone ◽  
Mariarosaria Bucci ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Shear Stress ◽  
Carotid Artery ◽  
Wistar Rats ◽  
Colorimetric Assay ◽  
Induced Hypertension ◽  
Effect Curve ◽  
Male Wistar Rats ◽  
H2s Production

Introduction: Glucocorticoid (GC) excess is related to hypertension. The deletion of endothelial GC-receptors abrogates the blood pressure increase, suggesting GC-induced hypertension is endothelium-dependent. In response to shear stress endothelium releases nitric oxide, endothelial derived hyperpolarizing factor (EDHF) and prostacyclin. Recently H2S has been proposed as a candidate for EDHF. H2S is mainly produced by the enzymes cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) from L-cysteine. The aim of this study was to investigate the EDHF/H2S signaling in GC-hypertension. Methods: Male Wistar rats were treated with DEX (1.5 mg/kg/sc) or vehicle (VEH) for 8 days. Systolic blood pressure (SBP) was monitored every 2 days. EDHF was evaluated in mesenteric plexus and carotid artery performing a concentration-effect curve of acetylcholine in presence of indomethacin (INDO) and nitro-L-arginine methyl ester (L-NAME). Apamin (APA) plus charibdotoxin (CTX), SKCa and BKCa inhibitors, or propargylglycine (PAG), CSE inhibitor, were used. CBS and CSE levels were analyzed by immunoblot. H2S levels were measured by a colorimetric assay. Results: DEX treatment significantly increased SBP compared to VEH (*p<0.05, **p<0.01, ***p<0.001 at days 2-4, 6, 8 respectively). EDHF-mediated relaxation of mesenteric bed or carotid artery was markedly reduced in DEX group compared to VEH (***p<0.001). APA and CTX as well as PAG abolished EDHF-mediated relaxation in DEX or VEH group (***,°°°p<0.001 respectively). CBS and CSE levels were significantly reduced in mesenteric plexus and carotid artery in DEX group (*p<0.05). The H2S production was markedly reduced in mesenteric plexus and carotid artery (*p<0.05, **p<0.01 respectively) as well as plasmatic H2S levels (*p<0.05) in DEX rats compared to VEH. Conclusions: Our data demonstrate that GC-excess induces an impairment of H2S/EDHF signaling indicating an additional cause of GC-mediated hypertension.

Abstract 649: Endothelial-derived Sphingolipids Preserve Systemic Vascular Function And Blood Pressure

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Anna Cantalupo ◽  
Yi Zhang ◽  
Hideru Obinata ◽  
Syvain Galvain ◽  
Xiang-Cheng Jiang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Vascular Function ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Critical Event ◽  
Ang Ii ◽  
Serine Palmitoyltransferase ◽  
Induced Hypertension

Endothelial dysfunction is a critical event in many cardiovascular diseases including hypertension. Although lipid signaling is implicated in endothelial dysfunction and cardiovascular diseases, specific molecular mechanisms are poorly understood. Here we report a novel regulation of endothelial sphingolipid synthesis by Nogo-B, membrane protein of the endoplasmic reticulum that modulates local sphingolipid production with direct effects on vascular function and blood pressure. Nogo-B inhibits serine palmitoyltransferase, rate-limiting enzyme of the sphingolipid de novo synthesis, controlling endothelial sphingosine 1-phosphate production and its autocrine G-protein-coupled receptor-dependent signaling actions. Mice lacking Nogo-B are hypotensive (90.1±1.6 vs. 119.9±2.6 mmHg WT mice), resistant to Ang-II (500ng/Kg/min)-induced hypertension (150.4±2.5 vs. 108.4±1.5 mmHg, compared to WT mice, 24 days after AngII infusion), and preserve endothelial function and nitric oxide release. Pharmacological inhibition of serine palmitoyltransferase with myriocin in mice that lack Nogo-B reinstated endothelial dysfunction and Ang-II-induced hypertension (143.9±1.5 vs. 90.1±1.6 mmHg, myriocin vs. vehicle treated Nogo-A/B-/- mice). Our study identifies Nogo-B as a key inhibitor of local sphingolipid synthesis and indicates that autocrine sphingolipids signaling within the endothelium are critical for vascular function and blood pressure homeostasis.

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