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Introduction: Excess sodium intake is common across all age, sex, racial, and ethnic groups in the US and remains an important modifiable risk factor for elevated blood pressure (BP), a leading contributor to cardiovascular disease. While multiple 24 -hour urinary measures of sodium excretion are the preferred objective measure of sodium intake, multiple standardized, interviewer-administered 24 hour dietary recalls offer a useful surrogate measure for longitudinal group comparisons, especially unique among US Hispanics/Latinos of diverse backgrounds. Objectives: To assess whether dietary sodium intake was associated with change in systolic blood pressure (SBP) over six years, overall and by use of BP lowering medication. Methods: The Hispanic Community Health Study/Study of Latinos is an ongoing prospective population-based study of 16,415 diverse Hispanics/Latinos aged 18-74 yr from four US communities. Visit 1 (baseline) was conducted in 2008-2011, and visit 2 is currently ongoing (2014-2017). Dietary sodium intake was averaged from two interviewer-administered 24-hour diet recalls collected at visit 1. Likewise, SBP was the average from three seated measurements in visit 1 and about six years later in visit 2. Change in SBP from visit 1 to visit 2 was calculated. Using linear regression models adjusted for age, sex, study site, follow-up years, Hispanic/Latino background, education, income, nativity, diabetes, chronic kidney disease, dyslipidemia, family history of CVD, BMI, smoking, alcohol use, physical activity, and energy intake, we estimated the association of a 500 mg/day increment of sodium intake on change in SBP. Models were further stratified by self-reported use of BP lowering medication at visit 2. Results: The sample includes 7,904 adults who attended visit 2 by September 2016; average follow-up time was 5.8 years (SE: 0.02). At visit 1 mean age was 44.5 years (SE: 0.05); 57% were female (SE: 0.86). Overall, mean sodium intake was 3171 mg/day (SE: 33); a 500 mg/day higher sodium intake was associated with a 0.33 mmHg increase in SBP (95% CI: 0.07, 0.60). Among individuals not reporting taking BP lowering medication, mean sodium was 3,181 (SE: 34) and a 500 mg higher sodium intake was associated with a non-significant 0.29 mmHg increase in SBP (95% CI: -0.00, 0.58). Among individuals on BP lowering medication, mean sodium intake was 2,966 (SE: 50) and a 500 mg higher sodium intake was significantly associated with a 0.61 mmHg increase in SBP (95% CI: 0.11, 1.11). Conclusions: Among a large sample of diverse US Hispanics/Latinos, higher sodium intake was associated with small SBP increases in approximately six years. The effect of sodium on elevated SBP was stronger among individuals on BP lowering medications. [ABSTRACT FROM AUTHOR]

Epidemilogical studies have established the role of cigarette smoking as a risk factor in the progression of chronic kidney disease, including diabetic nephropathy. We have previously reported that nicotine promotes mesangial cell proliferation and hypertrophy via activation of nonneuronal nicotinic acetylcholine receptors and that nicotine worsens renal injury in a model of acute glomerulonephritis (Jaimes E, Tian RX, RaJj L. Am J Physiol Heart Circ Physiol 292: H76-H82, 20 Jaimes EA, Tian RX, Joshi M, Raij L. Am J Nephrol 29: 319-326 2009). These studies were designed to test the hypothesis that nicotine worsens renal injury in db/db mice, a well-established model of diabetic nephropathy, and that reactive oxygen species play an important as mediators of these effects. For these studies, nicotine (100 µg/ml) was administered in the drinking water to control and db/db mice for 10 wk. Blood pressure was measured by the tail-cuff method, and urine was collected for proteinuria. At death, kidneys were collected for histology and molecular biology. The administration of nicotine did not result in significant changes in blood pressure or blood glucose and resulted in cotinine levels similar to those found in the plasma of smokers. In diabetic mice, the administration of nicotine significantly increased urinary protein excretion (1-fold), glomerular hypertrophy, and mesangial area (-20%). These changes were accompanied by significant increases in NADPH oxidase 4 (~30%) and increased nitrotyrosine and Akt expression. In vitro, we determined that nicotine has additive effects to high glucose on reactive oxygen species generation and Akt phosphorylation in human mesangial cells. These findings unveil novel mechanisms that may result in the development of novel strategies in the treatment and prevention of diabetic nephropathy in smokers. [ABSTRACT FROM AUTHOR]