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Background: Although the subject of numerous studies, the associations between dietary sodium, potassium, and the ratio of dietary sodium to potassium with blood pressure are not clear-cut. In addition, there is a paucity of research on these relationships in prospective cohort studies with representation from diverse Hispanic/Latino adults., Objectives: To evaluate the associations between dietary intake of sodium, potassium, and the ratio of dietary sodium to potassium and blood pressure in a diverse sample of Hispanics living in the United States., Methods: This analysis included 11,429 Hispanic/Latino participants of the prospective cohort Hispanic Community Health Study/Study of Latinos recruited between 2008 and 2011 in visit 1 who participated in a follow-up visit in 2014-2017. Dietary sodium and potassium intakes were averaged from 2 interviewer-administered 24-h diet recalls collected at visit 1. At both visits, blood pressure was measured 3 times in a seated position and averaged. We assessed the relationship between dietary sodium, potassium, and the sodium-to-potassium ratio with changes in systolic and diastolic blood pressure using survey-weighted multivariable-adjusted regression models., Results: At visit 1, the mean age was 41 y, and the mean sodium intake was 3203 mg/d. Each 500 mg/d sodium increment in intake was associated with an increase in systolic blood pressure (β: 0.35 [mmHg]; 95% confidence interval: 0.06, 0.63) and diastolic blood pressure (β: 0.45 [mmHg]; 95% confidence interval: 0.08, 0.82). Dietary potassium and the molar ratio of dietary sodium to potassium were not associated with changes in systolic or diastolic blood pressure., Conclusions: Among a large sample of diverse United States Hispanic/Latino adults, higher sodium intake was associated with small increases in systolic blood pressure over 6 y. This research underscores the importance of dietary sodium reduction in maintaining lower blood pressure., (Copyright © 2024 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

Background Among US Hispanics/Latinos, the largest ethnic minority population in the United States, hypertension incidence has not been thoroughly reported. The goal of this study was to describe the incidence of hypertension among US Hispanic/Latino men and women of diverse Hispanic/Latino background. Methods and Results We studied 6171 participants of the Hispanic Community Health Study/Study of Latinos, a diverse group of self-identified Hispanics/Latinos from 4 US urban communities, aged 18 to 74 years, and free from hypertension in 2008 to 2011 and re-examined in 2014 to 2017. Hypertension was defined as self-reported use of anti-hypertension medication, or measured systolic blood pressure ≥130 mm Hg, or diastolic blood pressure ≥80 mm Hg. Results were weighted given the complex survey design to reflect the target population. Among men, the 6-year age-adjusted probability of developing hypertension was 21.7% (95% CI, 19.5-24.1) and differed by Hispanic/Latino background. Specifically, the probability was significantly higher among men of Cuban (27.1%; 95% CI, 20.2-35.2) and Dominican (28.1%; 95% CI, 19.5-38.8) backgrounds compared with Mexican Americans (17.6%; 95% CI: 14.5-21.2). Among women, the 6-year age-adjusted probability of developing hypertension was 19.7% (95% CI, 18.1-21.5) and also differed by Hispanic/Latino background. Specifically, the probability was significantly higher among women of Cuban (22.6%; 95% CI, 18.3-27.5), Dominican (23.3%; 95% CI, 18.0-29.5), and Puerto Rican (28.2%; 95% CI, 22.7-34.4) backgrounds compared with Mexican Americans (16.0%; 95% CI, 13.9-18.4). Conclusions Hypertension incidence varies by Hispanic/Latino background, with highest incidence among those of Caribbean background.

Background: The prevention and control of hypertension is an essential component for reducing the burden of cardiovascular diseases. Here we describe the prevalence of hypertension in diverse Hispanic/Latino background groups and describe the proportion who are aware of their diagnosis, receiving treatment, and having their hypertension under control., Methods: The Hispanic Community Health Study/Study of Latinos is a longitudinal cohort study of 16,415 Hispanics/Latinos, aged 18-74 years from 4 US communities (Bronx, NY; Chicago, IL; Miami, FL; and San Diego, CA). At baseline (2008-2011) the study collected extensive measurements and completed questionnaires related to research on cardiovascular diseases. Hypertension was defined as measured blood pressure ≥140/90mm Hg or use of antihypertensive medication., Results: The total age-adjusted prevalence of hypertension in this study was 25.5% as compared with 27.4% in non-Hispanic whites in the National Health and Nutrition Examination Survey. Prevalence of hypertension increased with increasing age groups and was highest in Cuban, Puerto Rican, and Dominican background groups. The percent with hypertension who were aware, being treated with medication, or had their hypertension controlled was lower compared with US non-Hispanic whites with hypertension and it was lowest in those without health insurance., Conclusions: These findings indicate a significant deficit in treatment and control of hypertension among Hispanics/Latinos residing in the United States, particularly those without health insurance. Given the relative ease of identification of hypertension and the availability of low-cost medications, enabling better access to diagnostic and treatment services should reduce the burden of hypertension in Hispanic populations.

Purpose of Review: Vascular stiffening is a hallmark of the aging process. Improvements in the methods used to measure central stiffness, particularly applanation tonometry, and their use as therapeutic targets have generated great interest., Recent Findings: Vascular stiffness is associated with increases in pulse pressure (PP), aortic augmentation index, and pulse wave velocity (PWV). This last has emerged as the gold standard for evaluation of vascular stiffness, as it is an independent predictor of coronary heart disease, stroke, and mortality. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and calcium-channel blockers with or without diuretics are all commonly used to ameliorate vascular stiffness; however, selective β-1 blockers (β-blockers) may actually worsen aortic PP and aortic augmentation index., Summary: Serial measurements of vascular stiffness, including PWV, augmentation index, and PP, may be especially beneficial in older patients to supplement brachial blood pressure. At present, given the lack of universally accepted normal values for vascular stiffness as measured by applanation tonometry, serial measurements over time may be more helpful than a single isolated value. In patients with suspected vascular stiffening, therapy should include inhibition of the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs, calcium-channel blockers, and diuretics as needed to normalize blood pressure. β-Blockers should be reserved for patients with a history of myocardial infarction or congestive heart disease. It remains to be established whether β-blockers with vasodilator properties could improve the assessment of vascular compliance.

Angiotensin (Ang) II exerts its important physiologic functions through two distinct receptor subtypes, the type 1 (AT1) and type 2 (AT2) receptors. AT1 and AT2 receptors have demonstrated counterregulatory interactions in the cardiovascular and renal systems. The cross-talk between AT1 and AT2 receptors has been suggested to participate in regulating blood pressure, cardiovascular growth, fibrosis, and remodeling, as well as renal blood flow, growth, fibrosis, and sodium excretion. The AT1 receptor is distributed ubiquitously and abundantly in adult tissues, whereas expression of the AT2 receptor is high in the fetus but low in adult tissues. However, mounting evidence indicates that AT2 receptor cardiovascular expression increases in response to injury and AT1 receptor blocker therapy. This article reviews recent experimental and clinical data elucidating the role of the AT2 receptor in cardiovascular and renal homeostasis.

Objectives: Increased endothelial production of reactive oxygen species and decreased nitric oxide bioactivity, associated with the upregulation of monocyte chemoattractant protein (MCP)-1 and lectin-like oxidized low-density lipoprotein receptor (LOX)-1, link hypertension with atherogenesis. We investigated whether the beneficial effects of thiazide diuretics are exclusively related to a reduction in the biomechanical stress of hypertension or are also endowed with pleiotropic vasculoprotective effects that are independent of their effect upon blood pressure., Methods: Dahl salt-sensitive (DSS) rats, a paradigm of human salt-sensitive hypertension, were given a diet with normal salt (0.5% NaCl), high salt (4% NaCl), or a high salt diet plus either hydrochlorothiazide 75 mg/l, chlorthalidone 37 or 75 mg/l in their drinking water for 6 weeks. We determined systolic blood pressure (SBP), left ventricular hypertrophy (LVH), proteinuria, aortic superoxide anion (O2(-)) production, endothelium-dependent relaxation (EDR) to acetylcholine, and aortic angiotensin II type 1 (AT1) receptor, LOX-1, and MCP-1 messenger RNA expression (by real-time polymerase chain reaction)., Results: DSS rats on a high salt diet developed hypertension, LVH, proteinuria, increased production of aortic O2(-) (106%), impaired EDR, and aortic upregulation of AT1 receptor (198%), LOX-1 (135%), and MCP-1 (145%). Hydrochlorothiazide as well as the high and low dose of chlorthalidone reduced SBP, LVH, and proteinuria, but did not reduce O2(-) production, AT1 receptor, LOX-1, or MCP-1 expression, or improved EDR., Conclusions: This study demonstrates that thiazide diuretics do not reduce oxidative stress, improve endothelial function, or prevent the expression of pro-atherogenic molecules. We conclude that thiazide diuretics may not fully provide long-term global cardiovascular protection beyond lowering blood pressure.

Salt sensitivity of blood pressure is associated with an elevated risk of developing hypertension (HTN) and is an independent risk factor for cardiovascular disease. The prevalence of HTN increases after menopause. The aim of this study was to investigate prospectively whether the loss of ovarian hormones increases the occurrence of salt sensitivity among healthy premenopausal women. We enrolled 40 normotensive, nondiabetic women (age 47.2+/-3.5), undergoing hysterectomy-oophorectomy for nonneoplastic processes and not on hormone replacement, to determine the effect of changes in sodium intake on blood pressure the day before and subsequently 4 months after surgical menopause. Salt loading was achieved using a 2-L normal saline infusion and salt depletion produced by 40 mg of intravenous furosemide. A decrease >10 mm Hg in systolic blood pressure between salt loading and salt depletion was used to define salt sensitivity. Before and after menopause, salt-sensitive women exhibited higher waist/hip and waist/thigh ratios (P<0.01). Although all of the women remained normotensive, the prevalence of salt sensitivity was significantly higher after surgical menopause (21 women; 52.5%) than before (9 women; 22.5%; P=0.01), because 12 (38.7%) salt-resistant women developed salt sensitivity after menopause. In summary, we demonstrated that the prevalence of salt sensitivity doubled as early as 4 months after surgical menopause, without an associated increase in blood pressure. Epidemiological studies indicate that development of HTN may not occur until 5 to 10 years after menopause. The loss of ovarian hormones may unmask a population of women prone to salt sensitivity who, with aging, would be at higher risk for the subsequent development of HTN and cardiovascular disease.

Endothelial dysfunction (ED) complicates hypertension and is a precursor of atherosclerosis. Reduced NO bioactivity, because of increased reduced NAD(P)H oxidase-derived reactive oxygen species (ROS), plays a critical role in ED. gp91phox, predominantly expressed in the endothelium and adventitia, is a subunit of NAD(P)H oxidase important for its activation in response to angiotensin (Ang) II. Human atherosclerotic plaques are heavy laden with gp91phox. We have shown that in Dahl salt-sensitive (DS) rats, a paradigm of low renin salt-sensitive (SS) hypertension in humans, Ang II receptor blockade normalizes ROS production and endothelium-dependent relaxation (EDR) without significantly affecting systolic blood pressure (SBP). To additionally elucidate the mechanisms involved in the functional association of Ang II in SS hypertension, we administered a cell-permeable inhibitor of the assembly of p47phox with gp91phox in NAD(P)H oxidase, gp91ds-tat (10 mg/kg body weight, 3 weeks by minipump), to DS rats fed a 4% salt diet. Control rats received either vehicle or an inactive scramb-tat peptide. Vehicle-treated DS developed hypertension (SBP 168+/-5 mm Hg), left ventricular hypertrophy (LVH), proteinuria, impaired EDR, and increased aortic ROS production (superoxide 115% and peroxynitrite 157%) and expression of the proatherogenic molecules LOX-1 (130%) and MCP-1 (166%). gp91ds-tat, but not scramb-tat, normalized ROS and EDR, as well as LOX-1 and MCP-1, despite nonsignificant effects on SBP (159+/-5 mm Hg; P>0.05), left ventricular hypertrophy, and proteinuria. Our findings support the notion that in SS hypertension, activation of NAD(P)H oxidase promotes ED and atherogenesis via decreased nitric oxide bioactivity and increased LOX-1 and MCP-1, independent of blood pressure.

BACKGROUND High sodium and low potassium consumption are risk factors for hypertension. The objectives of this study were to describe usual daily intake of sodium and potassium among US Hispanics/Latinos of diverse background groups and estimate the proportion meeting guidelines for dietary sodium and potassium intake. METHODS We studied 16,171 participants of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), a diverse group of self-identified Hispanics/Latinos aged 18–74 years from 4 US communities. In 2008–2011, all HCHS/SOL participants underwent a standardized examination. Median usual daily intake of dietary sodium and potassium were derived from two 24-hour diet recalls; standard errors and 95% confidence intervals (CIs) were calculated using boot strap methods. Meeting 2015 US Department of Agriculture guidelines was defined as an intake of <2,300 mg/day of sodium and ≥4,700 mg/day of potassium. RESULTS Among US Hispanics/Latinos, median usual daily intake of sodium was 2,574 mg (95% CI: 2,547, 2,600) among women and 3,747 mg (95% CI: 3,697, 3,796) among men. Median usual daily intake of potassium was 2,069 mg (95% CI: 2,046, 2,092) among women and 2,649 mg (95% CI: 2,615, 2,683) among men. Overall, only 21.3% (95% CI: 20.2%, 22.4%) of the US Hispanic/Latino population met 2015 recommendations for sodium and 0.6% (95% CI: 0.4%, 0.8%) for potassium. CONCLUSIONS Among US Hispanics/Latinos intake of sodium is too high and potassium too low. Strategies to reduce sodium intake while simultaneously increasing intake of potassium in this US population are warranted. [ABSTRACT FROM AUTHOR]

BACKGROUND Current treatment for the secondary prevention of cardiovascular diseases frequently involves the prescription of several combination therapies, particularly antihypertensive medications and HMG-CoA reductase inhibitor. We have previously shown that in salt-sensitive hypertension either a statin or the calcium channel blocker amlodipine (Aml) have vasoprotective effects. Here, we investigated in aortas from Dahl salt-sensitive (DS) rats the effects of Aml, the statin atorvastatin (AT), and their combination on endothelial function, superoxide (O2−) production, and the expression of endothelial nitric oxide synthase (eNOS), chemokine monocyte chemoattractant protein-1 (MCP-1), and lectin-like oxidized LDL receptor-1 (LOX-1). METHODS Groups of DS rats were fed either normal-salt (NS, 0.5% NaCl) or high-salt (HS, 4% NaCl) diet or a HS diet with AT (15mg/kg/day), Aml (5mg/kg/day) or combination of AT/Aml for 6 weeks. RESULTS Rats on the HS diet developed hypertension, aortic hypertrophy, accompanied by increased plasma C-reactive protein (CRP), aortic O2−, MCP-1 (80%), and LOX-1 (55%) expression and reduced eNOS and endothelial-dependent relaxation to acetylcholine (EDR). Aml reduced systolic blood pressure (SBP), aortic hypertrophy, plasma CRP, vascular O2−, and MCP-1 expression and improved eNOS and EDR. AT reduced aortic hypertrophy and plasma CRP, improved EDR, and normalized vascular O2−, eNOS, and proinflammatory gene expression with mild reduction in SBP. Combination therapy further reduced the SBP and normalized aortic hypertrophy, EDR, and plasma CRP. CONCLUSIONS The combination therapy of Aml/AT has an additive beneficial effect on the vasculature. These novel findings may provide scientific basis for the combination therapy of statins with antihypertensive agents to reduce and prevent cardiovascular diseases. [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]

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]