scholarly journals High salt intake reduces nitric oxide‐dependent control of arteriolar tone in the mouse

2006 ◽  
Vol 20 (5) ◽  
Author(s):  
Timothy R. Nurkiewicz ◽  
Matthew A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Intake ◽  
Arteriolar Tone

Limitation of arteriolar myogenic activity by local nitric oxide: segment-specific effect of dietary salt

1999 ◽  
Vol 277 (5) ◽  
pp. H1946-H1955 ◽  
Author(s):  
Timothy R. Nurkiewicz ◽  
Matthew A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Salt Intake ◽  
Specific Effect ◽  
High Salt ◽  
Myogenic Response ◽  
Dietary Salt ◽  
No Donor ◽  
Spontaneously Hypertensive ◽  
High Salt Intake ◽  
Wistar Kyoto

The purpose of this study was to determine if local nitric oxide (NO) activity attenuates the arteriolar myogenic response in rat spinotrapezius muscle. We also investigated the possibility that hypertension, dietary salt, or their combination can alter any influence of local NO on the myogenic response. Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Mean arterial pressure was unaffected by dietary salt in WKY but was significantly higher and augmented by dietary salt in SHR. In all experiments, elevation of microvascular pressure by box pressurization caused a 0–30% decrease in the diameter of large (arcade bridge) arterioles and a 21–27% decrease in the diameter of intermediate (arcade) arterioles. Inhibition of NO synthase with N G-monomethyl-l-arginine (l-NMMA) significantly enhanced myogenic responsiveness of arcade bridge arterioles in WKY-LS and SHR-LS but not in WKY-HS and SHR-HS.l-NMMA significantly enhanced the myogenic responsiveness of arcade arterioles in all four groups. Excess l-arginine reversed this effect of l-NMMA in all cases, and arteriolar responsiveness to the NO donor sodium nitroprusside was not different among the four groups. High-salt intake had no effect on the passive distension of arterioles in either strain during box pressurization. We conclude that 1) local NO normally attenuates arteriolar myogenic responsiveness in WKY and SHR, 2) dietary salt impairs local NO activity in arcade bridge arterioles of both strains, and 3) passive arteriolar distensibility is not altered by a high-salt diet in either strain.

scholarly journals Maternal high-salt diet alters redox state and mitochondrial function in newborn rat offspring’s brain

2018 ◽  
Vol 119 (9) ◽  
pp. 1003-1011 ◽  
Author(s):  
Daniela P. Stocher ◽  
Caroline P. Klein ◽  
André B. Saccomori ◽  
Pauline M. August ◽  
Nicolli C. Martins ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Function ◽  
Redox State ◽  
Salt Intake ◽  
High Salt ◽  
Health State ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake ◽  
Pregnancy And Lactation

AbstractExcessive salt intake is a common feature of Western dietary patterns, and has been associated with important metabolic changes including cerebral redox state imbalance. Considering that little is known about the effect on progeny of excessive salt intake during pregnancy, the present study investigated the effect of a high-salt diet during pregnancy and lactation on mitochondrial parameters and the redox state of the brains of resulting offspring. Adult female Wistar rats were divided into two dietary groups (n 20 rats/group): control standard chow (0·675 % NaCl) or high-salt chow (7·2 % NaCl), received throughout pregnancy and for 7 d after delivery. On postnatal day 7, the pups were euthanised and their cerebellum, hypothalamus, hippocampus, prefrontal and parietal cortices were dissected. Maternal high-salt diet reduced cerebellar mitochondrial mass and membrane potential, promoted an increase in reactive oxygen species allied to superoxide dismutase activation and decreased offspring cerebellar nitric oxide levels. A significant increase in hypothalamic nitric oxide levels and mitochondrial superoxide in the hippocampus and prefrontal cortex was observed in the maternal high-salt group. Antioxidant enzymes were differentially modulated by oxidant increases in each brain area studied. Taken together, our results suggest that a maternal high-salt diet during pregnancy and lactation programmes the brain metabolism of offspring, favouring impaired mitochondrial function and promoting an oxidative environment; this highlights the adverse effect of high-salt intake in the health state of the offspring.

scholarly journals Dietary Salt With Nitric Oxide Deficiency Induces Nocturnal Polyuria via Hyperactivation of Intrarenal Angiotensin Ⅱ-SPAK-NCC Pathway

2021 ◽  
Author(s):  
Yosuke Sekii ◽  
Hiroshi Kiuchi ◽  
Kentaro Takezawa ◽  
Takahiro Imanaka ◽  
Sohei Kuribayashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Salt Intake ◽  
Underlying Mechanism ◽  
High Salt ◽  
Common Disease ◽  
No Production ◽  
Nocturnal Polyuria ◽  
Dietary Salt ◽  
High Salt Intake

Abstract Nocturnal polyuria is the most frequent cause of nocturia, a common disease associated with a compromised quality of life and increased mortality. Its pathogenesis is complex, and the detailed underlying mechanism remains unknown. Herein, we report that concomitant intake of a high-salt diet and reduced nitric oxide (NO) production achieved through Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) administration in mice resulted in nocturnal polyuria recapitulating the clinical features in humans. High salt intake under reduced NO production overactivated the angiotensin II-SPAK (STE20/SPS1-related proline–alanine-rich protein kinase)-NCC (sodium chloride co-transporter) pathway in the kidney, resulting in the insufficient excretion of sodium during the day and its excessive excretion at night. Excessive Na excretion at night in turn leads to nocturnal polyuria due to osmotic diuresis. Our study identified a central role for the intrarenal angiotensin II-SPAK-NCC pathway in the pathophysiology of nocturnal polyuria, highlighting its potential as a promising therapeutic target.

Effect of dietary salt on arteriolar nitric oxide in striated muscle of normotensive rats

1993 ◽  
Vol 264 (6) ◽  
pp. H1810-H1816 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Striated Muscle ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake ◽  
Low Salt ◽  
Induced Hypertension

This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.

Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake

2011 ◽  
Vol 301 (2) ◽  
pp. F263-F270 ◽  
Author(s):  
M. C. Fiore ◽  
P. M. Jimenez ◽  
D. Cremonezzi ◽  
L. I. Juncos ◽  
N. H. García
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Body Weight ◽  
Salt Intake ◽  
High Salt ◽  
Lipid Lowering ◽  
Inflammatory Factors ◽  
Glomerular Volume ◽  
High Salt Intake ◽  
Tgf Β1

High salt intake (HS) is a risk factor for cardiovascular and kidney disease. Indeed, HS may promote blood-pressure-independent tissue injury via inflammatory factors. The lipid-lowering 3-hydroxy 3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors exert beneficial lipid-independent effects, reducing the expression and synthesis of inflammatory factors. We hypothesized that HS impairs kidney structure and function in the absence of hypertension, and these changes are reversed by atorvastatin. Four groups of rats were treated for 6 wk in metabolic cages with their diets: normal salt (NS); HS, NS plus atorvastatin and HS plus atorvastatin. We measured basal and final body weight, urinary sodium and protein excretion (UProtV), and systolic blood pressure (SBP). At the end of the experimental period, cholesterolemia, creatinine clearance, renal vascular reactivity, glomerular volume, cortical and glomerular endothelial nitric oxide synthase (eNOS), and transforming growth factor (TGF)-β1 expression were measured. We found no differences in SBP, body weight, and cholesterolemia. HS rats had increased creatinine clearence, UProtV, and glomerular volume at the end of the study. Acetylcholine-induced vasodilatation decreased by 40.4% in HS rats ( P < 0.05). HS decreased cortical and glomerular eNOS and caused mild glomerular sclerosis, interstitial mononuclear cell infiltration, and increased cortical expression of TGF-β1. All of these salt-induced changes were reversed by atorvastatin. We conclude that long-term HS induces inflammatory and hemodynamic changes in the kidney that are independent of SBP. Atorvastatin corrected all, suggesting that the nitric oxide-oxidative stress balance plays a significant role in the earlier stages of salt induced kidney damage.

Uric acid is a key player in salt-induced endothelial dysfunction: the therapeutic role of Stigma maydis (corn silk) extract

2020 ◽  
Vol 45 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Adewumi Oluwafemi Oyabambi ◽  
Emmanuel Damilare Areola ◽  
Lawrence Aderemi Olatunji ◽  
Ayodele Olufemi Soladoye
Keyword(s):  
Nitric Oxide ◽  
Uric Acid ◽  
Salt Intake ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
High Salt ◽  
Corn Silk ◽  
High Salt Intake ◽  
Endothelial Nitric Oxide

Hyperuricemia has been implicated in the pathogenesis and complications of cardiovascular diseases with associated elevated oxidant events. There is evidence that excessive salt intake results in cardiometabolic disturbances but the mechanism is elusive. Also, Stigma maydis (corn silk) is noted for its antioxidant properties among other beneficial roles. This study, therefore, aimed to establish the effect of high-salt diet (SD) on uric acid (UA) production and the role of S. maydis in salt-induced phenotypes. Four groups of randomly selected rats (n = 5) were fed with normal rat feed, corn silk extract (500 mg/kg), SD (8%) and corn silk extract plus high-salt feed. After 6 weeks of the experimental procedure, each animal was anesthetized by exposure to chloroform vapor and blood samples collected by cardiac puncture. Data were expressed in means ± SEM and p values <0.05 were accepted as significant. SD resulted in reduced plasma superoxide dismutase (SOD), nitric oxide (NO), and glutathione peroxidase (GPx) but not endothelial nitric oxide synthase. Also, plasma UA and vascular cell adhesion molecule-1 (VCAM-1) increased in the SD group compared with control. However, S. maydis extract in the SD-exposed group increased NO and GPx and not SOD. Also, S. maydis extract attenuated UA and VCAM-1. In conclusion, high-salt intake may initiate deleterious cardiovascular events through UA-dependent mechanism and S. maydis extract has therapeutic potential in high-salt–induced oxidative damage and/or UA-dependent endothelial pathologies.

Flow-dependent arteriolar dilation in normotensive rats fed low- or high-salt diets

1995 ◽  
Vol 269 (4) ◽  
pp. H1407-H1414 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Vessel Occlusion ◽  
High Salt Intake ◽  
Significant Difference ◽  
Low Salt ◽  
No Release ◽  
Luminal Flow ◽  
Arteriolar Tone

Ingestion of a high-salt diet has previously been shown to suppress the endogenous influence of nitric oxide (NO) on arteriolar tone in hypertension-resistant, salt-resistant Dahl (SR/Jr) rats. Because luminal blood flow can be an important stimulus for endothelial NO release, this study was undertaken to determine whether high salt intake can also lead to a deficit in the direct flow-dependent regulation of arteriolar diameter. The spinotrapezius muscle microvasculature was studied by in vivo microscopy in SR/Jr rats fed low (0.45%)- or high (7%)-salt diets for 2 wk, and arcade arteriole responses to increased luminal flow (via parallel vessel occlusion) were studied in both dietary groups. There was no significant difference between groups in arterial pressure or in resting arteriolar diameters, volume flows, or wall shear rates. In low-salt SR/Jr, a 36% increase in luminal flow produced an average arteriolar dilation of 38% that was significantly reduced by the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). In high-salt SR/Jr, a similar flow increase produced an average dilation of only 16% (P < 0.05 vs. low-salt SR/Jr), and this response was unaffected by L-NMMA. Inhibition of cyclooxygenase activity with meclofenamate had no effect on this response in either group. These findings suggest that NO release mediates a portion of flow-dependent arteriolar dilation in rat spinotrapezius muscle and that high salt intake, in the absence of hypertension, can attenuate this response via a suppression of NO activity.

Deletion of cyclooxygenase-2 in the mouse increases arterial blood pressure with no impairment in renal NO production in response to chronic high salt intake

2013 ◽  
Vol 304 (10) ◽  
pp. R899-R907 ◽  
Author(s):  
Mette Stæhr ◽  
Pernille B. L. Hansen ◽  
Kirsten Madsen ◽  
Paul M. Vanhoutte ◽  
Rolf M. Nüsing ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Salt Intake ◽  
High Salt ◽  
No Production ◽  
Arterial Blood ◽  
High Salt Intake ◽  
Cox 2

Experiments were designed to test the hypothesis that cyclooxygenase-2 (COX-2) activity attenuates the blood pressure increase during high NaCl intake by stimulation of endothelial nitric oxide synthase (eNOS)-mediated NO synthesis in the kidney medulla. COX-2−/− (C57BL6) an COX-2+/+ mice were fed a diet with 0.004% (low salt, LS) or 4% (high salt, HS) NaCl for 18 days. Arterial blood pressure was recorded continuously using indwelling catheters. Food and water intake and diuresis were measured in metabolic cages. Urine osmolality and excretion of electrolytes, cGMP, cAMP, and NOx were determined, as well as plasma NOx and cGMP. There was a significant dependence of blood pressure on salt intake and genotype: COX-2−/− exhibited higher blood pressure than COX-2+/+ both on HS and LS intake. COX-2+/+ littermates displayed an increase in blood pressure on HS versus LS (102.3 ± 1.1 mmHg vs. 91.9 ± 0.9 mmHg) day and night. The mice exhibited significant blood pressure increases during the awake phase (night) that were larger in COX-2−/− on HS diet compared with COX-2+/+. Water intake, diuresis, Na+, and osmolyte excretions and NOx and cGMP excretions were significantly and similarly elevated with HS in COX-2−/− and COX-2+/+. In summary, C57BL6 mice exhibit a salt intake-dependent increase in arterial blood pressure with increased renal NO production. COX-2 activity has a general lowering effect on arterial blood pressure. COX-2 dampens NaCl-induced increases in arterial blood pressure in the awake phase. In conclusion, COX-2 activity attenuates the changes in nocturnal blood pressure during high salt intake, and COX-2 activity is not necessary for increased renal nitric oxide formation during elevated NaCl intake.

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