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The purpose of this study was to investigate the influence of dietary potassium on the sodium effect on blood pressure (BP) in the general population and the adherence of current recommendations for sodium and potassium intake. An overnight (12-hour) urine sample was collected in a population-based study to investigate cardiovascular risk. A sub-sample of 1285 subjects (age range, 25-64 years) free from any medication interfering with BP or potassium excretion was studied. Of the participants, 86.0% consumed over 6 g of salt/day and 87.7% less than the recommended intake of potassium (4.7 g). Potassium excretion and the sodium to potassium ratio were significantly related to systolic and diastolic BP only in subjects consuming more than 6 g/day of salt. Subjects in the highest sodium to potassium ratio quartile (surrogate of unhealthy diet) presented 8 mm Hg and 7 mm Hg higher values of systolic and diastolic BP, respectively, when compared with the first quartile, while individuals in the fourth quartile of urinary potassium excretion (healthier diet) showed 6 mm Hg and 4 mm Hg lower systolic and diastolic BP, respectively, compared with the first quartile. Our data indicate that when people have an increased intake of potassium, high intake of sodium is not associated with higher BP., (Copyright © 2014 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Objective: To analyze the posteffects of a single bout of resistance exercise on cardiovascular parameters in patients with peripheral artery disease (PAD)., Design: Randomized cross-over., Materials and Methods: Seventeen PAD patients performed two experimental sessions: control (C) and resistance exercise (R). Both sessions were identical (eight exercises, 3×10 repetitions), except that the R session was performed with an intensity between 5 and 7 in the OMNI-RES scale and the C session was performed without any load. Systolic blood pressure (BP), diastolic BP, heart rate, and rate-pressure product (RPP) were measured for 1 h after the interventions in the laboratory and during 24-h using ambulatory BP monitoring., Results: After the R session, systolic BP (greatest reduction: -6±2 mmHg, P<0.01) and RPP (greatest reduction: -888±286 mmHg×bpm; P<0.01) decreased until 50 min after exercise. From the second hour until 23 h after exercise, BP, heart rate, and RPP product were similar (P>0.05) between R and C sessions. BP load, nocturnal BP fall, and morning surge were also similar between R and C sessions (P>0.05)., Conclusion: A single bout of resistance exercise decreased BP and cardiac work for 1 h after exercise under clinical conditions, and did not modify ambulatory cardiovascular variables during 24 h in patients with PAD.

Background: The aim of this study was to investigate the effects of chronic treatment with carvedilol in blood pressure (BPV) and heart rate (HRV) variability of rats with myocardial infarction (MI)., Methods: MI was produced in male rats by ligature of anterior interventricular branch of left coronary artery. Control rats were submitted to a sham surgery (SO). MI and SO rats were randomized to receive for 30 days placebo (Plac 0.5% metilcelulose) or carvedilol (Carv, 2mg/Kg body weight/day, drinking water): SO-Plac (N = 10), SO-Carv (N = 10), MI-Plac (N = 12), MI-Carv (N = 13). Blood pressure (BP) was directly recorded in the awake animals and BPV was determined, in time (variance, mmhg(2)) and frequency domains by the autoregressive method. Statistical significance was set in P<0.05. Data are median and interquartile range., Results: No significant changes in HRV was observed in MI rats, while BPV showed significant decreasing of blood pressure variance (SO-Plac = 42.08 (39.21) mmHg(2) vs. MI-Plac = 21.67 (12.58) mmHg(2), P<0.05), reversed by the Carv treatment (MI-Plac = 21.67 (12.58) vs. MI-Carv = 38.64 (29.25), P<0.05). In the frequency domain analyses, MI reduced absolute and normalized LF component (LF (mmHg(2)): SO-Plac = 8.98 (14.84) vs. MI-Plac = 2.08 (4.84), P<0.05; LF(nu): SO-Plac = 79.48 (45.03) nu vs. MI-Plac = 24.25 (40.67) nu, P<0.05) and increased the normalized HF component of the BPV (SO-Plac = 20.51 (39.18) vs. MI-Plac = 60.51 (39.73). Carv treatment significantly attenuated the LF component fall., Conclusion: Chronic treatment with carvedilol restored the variance of BPV altered by the MI., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Objective: To analyze the effect of a single bout of resistance exercise on cardiac autonomic modulation in patients with peripheral artery disease., Methods: Fifteen patients with peripheral artery disease (age: 58.3±4.0 years) underwent the following sessions in a random order: resistance exercise (three sets of 10 repetitions of the six resistance exercises with a workload of 5-7 in the OMNI-RES scale) and control (similar to the resistance session; however, the resistance exercises were performed with no load). The frequency domain (low frequency, high frequency and sympathovagal balance) and symbolic analysis (0V, 1V and 2V patterns) of heart rate variability were obtained before and until one hour after the interventions., Results: After the resistance exercise and control sessions, similar increases were observed in the consecutive heartbeat intervals (control: 720.8±28.6 vs. 790.9±34.4 ms; resistance exercise: 712.9±30.1 vs. 756.8±37.9 ms; p<0.05) and in the pattern of the symbolic analysis with no variation (0V) (control: 25.1±3.5 vs. 33.4±4.1%; resistance exercise: 26.1±3.2 vs. 29.7±3.5%; p<0.05) until 50 min after both interventions. The pattern of two variations (2V) decreased similarly (control: 11.2±2.1 vs. 8.3±2.1%; resistance exercise: 9.5±1.7 vs. 7.8±1.7%; p<0.05). In contrast, the pattern of one variation (1V), the low and high frequency bands and sympathovagal balance did not change after the interventions (p>0.05)., Conclusion: A single bout of resistance exercise did not alter cardiac autonomic modulation in patients with peripheral artery disease.

A high salt diet is a known risk factor for cardiovascular diseases that leads to cardiac hypertrophy and creates a substrate for arrhythmias and sudden death. However, acute arrhythmogenesis after infarction has not been studied. Male Wistar rats (21 days) received drinking water (MI) or 1% NaCl solution (MI-Salt-C) for 4 weeks. Water was given to another group for 4 weeks, and on the day before surgery, animals received a 1% NaCl solution (MI-Salt-A). Non-invasive systolic blood pressure (SBP) was obtained before surgery. Myocardial infarction (MI) was produced by permanent occlusion of the left coronary artery. Electrocardiogram was monitored during the first 30 min post-occlusion to evaluate arrhythmias. Although SBP was not altered by salt intake (SHAM: 114±2, MI: 112±2, MI-Salt-C: 115±2, MI-Salt-A: 116±4 mm Hg), ventricular hypertrophy was observed in the animals receiving chronic salt diet (SHAM: 0.22±0.008, MI: 0.23±0.007, MI-Salt-C: 0.28±0.01; MI-Salt-A: 0.23±0.01 g/cm; P<0.05). Ventricular premature beats increased in both salt-loaded groups compared to MI group (MI: 805±81, MI-Salt-C: 1145±98; MI-Salt-A: 1023±77; P<0.05). Atrioventricular blockade was only observed in animals subjected to high salt intake (MI-Salt-C: 38.9%; MI-Salt-A: 42.1%). High salt intake was associated with increased post-infarct arrhythmias; however, this effect was unrelated to ventricular hypertrophy., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

The aim of the present study was to evaluate the effect of low-dose spironolactone initiated during the early stages of hypertension development and to assess the effects of chronic pressure overload on ventricular remodeling in rats. Male spontaneously hypertensive rats (SHRs) (4 weeks) were randomized to receive daily spironolactone (20 mg/kg) or vehicle (mineral oil) from 4 weeks to 8 months of age. Systolic blood pressure was measured non-invasively by tail-cuff pletysmography at baseline, 4 and 8 months. Hemodynamic assessment was performed at the end of treatment by arterial and ventricular catheterization. An in situ left ventricular pressure-volume curve was created to evaluate dilatation and wall stiffness. Systolic blood pressure at 1 month of age was higher in SHRs than in the Wistar group; it increased throughout the follow-up period and remained elevated with treatment (Wistar: 136 ± 2, SHR: 197 ± 6.8, SHR-Spiro: 207 ± 7.1 mmHg; p < 0.05). Spironolactone reduced cardiac hypertrophy (Wistar: 1.25 ± 0.03 SHR: 1.00 ± 0.03, SHR-Spiro: 0.86 ± 0.02 g; p < 0.05) and left ventricular mass normalized to body weight (Wistar: 2.51 ± 0.06, SHR: 2.70 ± 0.08, 2.53 ± 0.07 mg/g; p < 0.05). Moreover, the left ventricular wall stiffness that was higher in SHRs was partially reduced by spironolactone treatment (Wistar: 0.370 ± 0.032; SHR: 0.825 ± 0.058; SHR-Spiro: 0.650 ± 0.023 mmHg/ml; p < 0.05). Our results show that long-term spironolactone treatment initiated at the early stage of hypertension development reduces left ventricular hypertrophy and wall stiffness in SHRs.

Background: Insulin resistance and obesity are recognized as left ventricular (LV) mass determinants independent of blood pressure (BP). Prevalence of LV hypertrophy (LVH) and the relationship between LV mass to body composition and metabolic variables were evaluated in normotensive individuals as participants of a population-based study., Methods: LV mass was measured using the second harmonic image by M-mode 2D guided echocardiography in 326 normotensive subjects (mean 47+/-9.4 years). Fasting serum lipids and glucose, BP, body composition and waist circumference (WC) were recorded during a clinic visit., Results: Applying a normalization criterion not related to body weight (g/height raised to the power 2.7) and the cut-off points of 47.7 (men) and 46.6 g/m(2.7) (women), LVH was found in 7.9% of the sample. Univariate analysis showed LV mass (g/m(2.7)) related to age, body mass index (BMI), WC, fat and lean body mass, systolic and diastolic BP, and metabolic variables (cholesterol, HDL-c, triglycerides and glucose). In multivariate analysis only BMI and age-adjusted systolic BP remained as independent predictors of LV mass, explaining 31% and 5% of its variability. Removing BMI from the model, WC, age-adjusted systolic BP and lean mass remained independent predictors, explaining 25.0%, 4.0% and 1.5% of LV mass variability, respectively. After sex stratification, LV mass predictors were WC (8%) and systolic BP (5%) in men and WC (36%) and systolic BP (3%) in women., Conclusion: BMI in general and particularly increased abdominal adiposity (WC as surrogate) seems to account for most of LV mass increase in normotensive individuals, mainly in women.