High-phosphorus/zinc-free diet aggravates hypertension and cardiac dysfunction in a rat model of the metabolic syndrome

Suzuki, Yuka; Mitsushima, Shingo; Kato, Atsushi; Yokota, Takanori; Ichihara, Sahoko

doi:10.1016/j.carpath.2013.06.004

Cited by 17 publications

(17 citation statements)

References 37 publications

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“…These results are in accordance with all but one 28 report in normotensive and spontaneously hypertensive rats (both with normal renal function), that an HP diet elevated BP and augmented the exercise pressor reflex function. [29][30][31] Our studies also offer an explanation-at least in part-of the mechanism of the phosphate-induced hypertensinogenic effect: Although plasma renin/aldosterone concentrations and 24-hour excretion rates for both aldosterone and free cortisol were unchanged, 24-hour urinary excretion rates of metanephrine and normetanephrine increased significantly, explaining the additional observation of significantly increased mean 24-hour pulse rate. Even small increases in sympathetic nervous system activity may be sufficient to cause significant hypertension because an HP diet in mice has been reported to potentiate phenylephrineinduced vasoconstriction in ex vivo aortic rings.…”

Section: Discussionmentioning

confidence: 60%

A Controlled Increase in Dietary Phosphate Elevates BP in Healthy Human Subjects

Mohammad

Scanni

Bestmann

et al. 2018

JASN

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Despite epidemiologic evidence for increased cardiovascular morbidity and mortality associated with both high dietary and serum phosphate in humans with normal renal function, no controlled phosphate intervention studies of systemic hemodynamics have been reported. Higher serum 25(OH) vitamin D levels are associated with better cardiovascular outcomes, but vitamin D increases intestinal phosphate absorption. We conducted a prospective outpatient study with blinded assessment in 20 young adults with normal renal function randomized to high phosphate (regular diet plus 1 mmol/kg body wt per day of Na as neutral sodium phosphate) or low phosphate (regular diet plus lanthanum, 750 mg thrice/day, plus 0.7 mmol/kg body wt per day of Na as NaCl) for 11 weeks. After 6 weeks, all subjects received vitamin D (600,000 U) by intramuscular injection. Outcome parameters were 24-hour ambulatory systolic and diastolic BP (SBP and DBP), pulse rate (PR), biomarkers, and measures of endothelial and arterial function. Compared with the low-phosphate diet group, the high-phosphate diet group had a significant increase in mean±SEM fasting plasma phosphate concentration (0.23±0.11 mmol/L); 24-hour SBP and DBP (+4.1; 95% confidence interval [95% CI], 2.1 to 6.1; and +3.2; 95% CI, 1.2 to 5.2 mm Hg, respectively); mean 24-hour PR (+4.0; 95% CI, 2.0 to 6.0 beats/min); and urinary metanephrine and normetanephrine excretion (54; 95% CI, 50 to 70; and 122; 95% CI, 85 to 159 g/24 hr, respectively). Vitamin D had no effect on any of these parameters. Neither high- nor low-phosphate diet nor vitamin D affected endothelial function or arterial elasticity. Increased phosphate intake (controlled for sodium) significantly increases SBP, DBP, and PR in humans with normal renal function, in part, by increasing sympathoadrenergic activity.

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Section: Discussionmentioning

confidence: 60%

A Controlled Increase in Dietary Phosphate Elevates BP in Healthy Human Subjects

Mohammad

Scanni

Bestmann

et al. 2018

JASN

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“…Suzuki and his coworkers found that in spontaneously hypertensive rats, high phosphate and zinc-free diet markedly reduced their left ventricular systolic and diastolic function and cause severe myocardial fibrosis histopathologically. 43 Liu et al described that high phosphate level is related with increased secretion of ANP and BNP in cardiac myoblast. 44 Hyperphosphate may cause cardiomyocytes abnormalities both in structural and functional.…”

Section: Discussionmentioning

confidence: 99%

Hemodialysis‐induced regional left ventricular systolic dysfunction

Nie

Zhang

Zou

et al. 2016

Hemodialysis International

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Introduction Hemodialysis (HD) patients are under observably elevated cardiovascular mortality. Cardiac dysfunction is closely related to death caused by cardiovascular diseases (CVD). In the general population, repetitive myocardial ischemia induced left ventricular (LV) dysfunction may progress to irreversible loss of contraction step by step, and finally lead to cardiac death. In HD patients, to remove water and solute accumulated from 48 or 72 hours of interdialysis period in a 4-hour HD session will induce myocardial ischemia. In this study, we evaluated the prevalence and potential risk factors associated with HD-induced LV systolic dysfunction and provide some evidences for clinical strategies. Methods We recruited 31 standard HD patients for this study from Fudan University Zhongshan hospital. Echocardiography was performed predialysis, at peak stress during HD (15 minutes prior to the end of dialysis), and 30 minutes after HD. Auto functional imaging (AFI) was used to assess the incidence and persistence of HD-induced regional wall motion abnormalities (RWMAs). Blood samples were drawn to measure biochemical variables. Findings Among totally 527 segments of 31 patients, 93.54% (29/31) patients and 51.40% (276/527) segments were diagnosed as RWMAs. Higher cTnT (0.060 ± 0.030 vs. 0.048 ± 0.015 ng/mL, P = 0.023), phosphate (2.07 ± 0.50 vs. 1.49 ± 0.96 mmol/L, P = 0.001), UFR (11.00 ± 3.89 vs. 8.30 ± 2.66 mL/Kg/h, P = 0.039) and lower albumin (37.83 ± 4.48 vs. 38.38 ± 2.53 g/L, P = 0.050) were found in patients with severe RWMAs (RWMAs in more than 50% segments). After univariate and multivariate analysis, interdialytic weight gain (IDWG) was found as independent risk factor of severe RWMAs (OR = 1.047, 95%CI 1.155-4.732, P = 0.038). Discussion LV systolic dysfunction induced by HD is prevalent in conventional HD patients and should be paid attention to. Patients would benefit from better weight control during interdialytic period to reduce ultrafiltration rate.

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“…З даних наукової літератури відомо, що рівень цинку в сітківці ока людини знижується з віком (вікова дегенерація жовтої плями) через мутації в генах, що беруть участь в підтримці гомеостазу сітківки [9].…”

Section: метаболічні ефекти цинку (огляд літератури)unclassified