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Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake.

ABSTRACT: Striatin is a protein regulator of vesicular trafficking in neurons that also binds caveolin-1 and Ca(2+)-calmodulin and could activate endothelial nitric oxide synthase. We have shown that striatin colocalizes with the mineralocorticoid receptor and that mineralocorticoid receptor activation increases striatin levels in vascular cells. To test whether striatin is a regulator of vascular function, wild-type and heterozygous striatin-deficient mice (Strn(+/-)) were randomized in crossover intervention to restricted (0.03%) and liberal sodium (1.6%) diets for 7 days on each diet, and blood pressure and aortic vascular function were measured. Compared with wild-type, sodium restriction significantly reduced blood pressure in Strn(+/-). On liberal salt intake, phenylephrine and high KCl caused a greater vascular contraction in Strn(+/-) than wild-type, and endothelium removal, nitric oxide synthase inhibitor L-NAME, and guanylate cyclase inhibitor ODQ enhanced phenylephrine contraction to a smaller extent in Strn(+/-) than wild-type. On liberal salt, acetylcholine relaxation was less in Strn(+/-) than in wild-type, and endothelium removal, L-NAME, and ODQ blocked acetylcholine relaxation, suggesting changes in endothelial NO-cGMP. On liberal salt, endothelial nitric oxide synthase mRNA expression and the ratio of endothelial nitric oxide synthase activator pAkt/total Akt were decreased in Strn(+/-) versus wild-type. Vascular relaxation to NO donor sodium nitroprusside was not different among groups. Thus, striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction, and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake.

SUBMITTER: Garza AE

PROVIDER: S-EPMC4537321 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake.

Garza Amanda E AE Pojoga Luminita H LH Moize Burhanuddin B Hafiz Wan M WM Opsasnick Lauren A LA Siddiqui Waleed T WT Horenstein Michael M Adler Gail K GK Williams Gordon H GH Khalil Raouf A RA

Hypertension (Dallas, Tex. : 1979) 20150713 3

Striatin is a protein regulator of vesicular trafficking in neurons that also binds caveolin-1 and Ca(2+)-calmodulin and could activate endothelial nitric oxide synthase. We have shown that striatin colocalizes with the mineralocorticoid receptor and that mineralocorticoid receptor activation increases striatin levels in vascular cells. To test whether striatin is a regulator of vascular function, wild-type and heterozygous striatin-deficient mice (Strn(+/-)) were randomized in crossover interve ...[more]

PMID: 26169051

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Project description:IntroductionAccurate sodium intake estimates in adults with elevated blood pressure are essential for monitoring salt reduction progress and preventing cardiovascular diseases. However, sodium assessments are challenging in this high-risk population because many commonly used antihypertensive drugs alter urinary sodium excretion. Despite the high cost and substantial participant burden of gold-standard 24-hour urine collection, the relative performance of existing spot-urine based equations and dietary self-report instruments have not been well studied in this population, who will benefit from salt restriction. This systematic review aims to describe the current methods of assessing dietary sodium intake in adults with elevated blood pressure and determine what method can provide a valid and accurate estimate of sodium intake compared with the gold standard 24-hour urine collection.Methods and analysisStudies assessing sodium intake in adults aged 18 years and above with reported elevated blood pressure will be included. Five electronic databases (MEDLINE, Embase, Global Health, WoS and Cochrane CENTRAL) will be systematically searched from inception to March 2021. Also, a manual search of bibliographies and grey literature will be conducted. Two reviewers will screen the records independently for eligibility. One reviewer will extract all data, and two others will review the extracted data for accuracy. The methodological quality of included studies will be evaluated based on three scoring systems: (1) National Heart, Lung and Blood Institute for interventional studies; (2) Biomarker-based Cross-sectional Studies for biomarker-based observational studies and (3) European Micronutrient Recommendation Aligned Network of Excellence for validation studies of dietary self-report instruments.Ethics and disseminationAs the proposed systematic review will collect and analyse secondary data associated with individuals, there will be no ethical approval requirement. Findings will be disseminated in a peer-reviewed journal or presented at a conference.Prospero registration numberCRD42020176137.

Project description:This study sought to determine the efficacy of dietary sodium restriction (DSR) for improving vascular endothelial dysfunction in middle-aged/older adults with moderately elevated systolic blood pressure (SBP) (130-159 mm Hg) and the associated physiological mechanisms.Vascular endothelial dysfunction develops with advancing age and elevated SBP, contributing to increased cardiovascular risk. DSR lowers BP, but its effect on vascular endothelial function and mechanisms involved are unknown.Seventeen subjects (11 men and 6 women; mean age, 62 ± 7 years) completed a, randomized crossover study of 4 weeks of both low (DSR) and normal sodium intake. Vascular endothelial function (endothelium-dependent dilation; EDD), nitric oxide (NO)/tetrahydrobiopterin (BH(4)) bioavailability, and oxidative stress-associated mechanisms were assessed following each condition.Urinary sodium excretion was reduced by ? 50% (to 70 ± 30 mmol/day), and conduit (brachial artery flow-mediated dilation [FMD(BA)]) and resistance (forearm blood flow responses to acetylcholine [FBF(ACh)]) artery EDD were 68% and 42% (peak FBF(ACh)) higher following DSR (p < 0.005). Low sodium markedly enhanced NO-mediated EDD (greater ?FBF(ACh) with endothelial NO synthase inhibition) without changing endothelial NO synthase expression/activation (Ser 1177 phosphorylation), restored BH(4) bioactivity (less ?FMD(BA) with acute BH(4)), abolished tonic superoxide suppression of EDD (less ?FMD(BA) and ?FBF(ACh) with ascorbic acid infusion), and increased circulating superoxide dismutase activity (all p < 0.05). These effects were independent of ?SBP. Other subject characteristics/dietary factors and endothelium-independent dilation were unchanged.DSR largely reversed both macro- and microvascular endothelial dysfunction by enhancing NO and BH(4) bioavailability and reducing oxidative stress. Our findings support the emerging concept that DSR induces "vascular protection" beyond that attributable to its BP-lowering effects.

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Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake.

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Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake.

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