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Short-term cardiovascular regulation mediated by the sympathetic and parasympathetic branches of the autonomic nervous system has been investigated by multivariate autoregressive (MVAR) modeling, providing insightful analysis. MVAR models employ, as inputs, heart rate (HR), systolic blood pressure (SBP) and respiratory waveforms. ECG (from which HR series is obtained) and respiratory flow waveform (RFW) can be easily sampled from the patients. Nevertheless, the available methods for acquisition of beat-to-beat SBP measurements during exams hamper the wider use of MVAR models in clinical research. Recent studies show an inverse correlation between pulse wave transit time (PWTT) series and SBP fluctuations. PWTT is the time interval between the ECG R-wave peak and photoplethysmography waveform (PPG) base point within the same cardiac cycle. This study investigates the feasibility of using inverse PWTT (IPWTT) series as an alternative input to SBP for MVAR modeling of the cardiovascular regulation. For that, HR, RFW, and IPWTT series acquired from volunteers during postural changes and autonomic blockade were used as input of MVAR models. Obtained results show that IPWTT series can be used as input of MVAR models, replacing SBP measurements in order to overcome practical difficulties related to the continuous sampling of the SBP during clinical exams.

In patients with severe autonomic dysfunction, water ingestion elicits an acute pressor response. Hypertension may be associated with changes in cardiovascular autonomic modulation, but there is no information on the acute effects of water ingestion in patients with hypertension. In this study, we compared the effect of acute water ingestion on haemodynamic and autonomic responses of hypertensive and normotensive individuals. Eight patients with mild hypertension were compared to 10 normotensive individuals. After 30 min resting in the supine position all subjects ingested 500 ml of water. At baseline and after water ingestion, venous blood samples for plasma volume determination were collected, and electrocardiographic tracings, finger blood pressure, forearm blood flow and muscle sympathetic nerve activity (MSNA) were obtained. Water ingestion resulted in similar and minor reduction in plasma volume. Systolic and diastolic blood pressure increased in both hypertensive (mean+/-s.d.: 19/14+/-6/3 mm Hg) and normotensive subjects (17/14+/-6/3 mm Hg). There was an increase in forearm vascular resistance and in MSNA. Heart rate was reduced (hypertensive: 5+/-1 beats/min, normotensive: 5+/-6 beats/min) and the high-frequency component of heart rate and systolic blood pressure variability was increased. In hypertensive and normotensive individuals, acute water ingestion elicits a pressor response, an effect that is most likely determined by an increased vasoconstrictor sympathetic activity, and is counterbalanced by an increase in blood pressure and heart rate vagal modulation.

The aim of this study was to determine the contribution of NO to arterial pressure and heart rate variability in normotensive rats subjected to high sodium intake. Arterial pressure, heart rate, and arterial pressure and heart rate variability, baroreflex sensitivity, and pressure responsiveness were measured in male Wistar rats treated for 6 weeks (control and high sodium [1%] intake groups), before and after acute NO synthesis blockade. After treatment, no changes were observed in arterial pressure or heart rate. Arterial pressure variability was increased after sodium intake; however, heart rate variability and baroreflex sensitivity were not modified in high-sodium rats. NO synthase blockade increased arterial pressure in both groups but was higher in the high-sodium group (from 110+/-5 to 162+/-1.5 mm Hg) compared with the control group (from 109+/-6.7 to 144+/-10 mm Hg). The increase in arterial pressure was accompanied by a decrease in heart rate (from 354+/-28 to 303+/-25 bpm in control rats and from 380+/-34 to 298+/-30 bpm in high-sodium rats). NO synthase blockade increased the tachycardic response to sodium nitroprusside in high-sodium rats. Arterial pressure variability, evaluated by a nonlinear method (3D return maps), showed a larger reduction in response to NO synthase inhibition in the high-sodium group (from 162+/-26 to 34.8+/-8.6 for general index of beat-to-beat blood pressure variability) than in the control group (from 58+/-9.6 to 36+/-4.7 for general index of beat-to-beat blood pressure variability). Heart rate variability, evaluated by the SD of the R-R intervals, was not changed in control rats but was increased by NO synthase inhibition in the high-sodium rats (from 9.5+/-0.2 to 21.9+/-1.7 milliseconds). These findings suggest an important role for increased NO production in adaptation to high-sodium intake. The increase in NO system sensitivity in high-sodium intake may contribute to changes in the autonomic nervous system regulating heart rate and, especially, arterial pressure variability.

Objective: To analyze the role of autonomic function and other possible factors associated with a blunted fall in nocturnal blood pressure., Research Design and Methods: A total of 39 normotensive normnoalbuminuric type 1 diabetic patients were studied. Glomerular filtration rate (51Cr-EDTA technique), extracellular volume (51Cr-EDTA distribution volume), and urinary albumin excretion rate (UAER) (by radioimmunoassay) were measured. The subjects' 24-h ambulatory blood pressure and a 24-h electrocardiogram were recorded simultaneously Heart rate variability was calculated in the time domain for 24 h, in the frequency domain at night, at rest in the supine position, and during tilt. Patients were classified according to diastolic blood pressure (dBP) night/day ratio as dipper patients (< or =0.9) and nondipper patients (>0.9)., Results: Nondipper patients presented a higher low-frequency (LF) component (a sympathetic index) and higher LF/high-frequency (HF) ratio during sleep than dipper patients (0.29 +/- 0.12 vs. 0.19 +/- 0.10 normalized units [n.u.], P = 0.008; and 0.98 +/- 0.53 vs. 0.55 +/- 0.45 n.u., P = 0.007, respectively). At rest, the LF component in nondipper patients (0.38 +/- 0.13 n.u.) was higher than in dipper patients (0.27 +/- 0.12 n.u., P = 0.04). After the tilt, nondipper patients did not show an increase in the LF component (P = 0.32), but in dipper patients, the increase was significant (P = 0.001). In both groups, tilting promoted a decrease in the HF component (a parasympathetic index). In a stepwise multiple linear regression analysis, the LF component during sleep and the UAER accounted for 24% of the variability in the dBP night/day ratio., Conclusions: The predominance of sympathetic activity and increased levels of UAER, although within the normal range, are associated with a blunted fall in nocturnal dBP in normoalbuminuric normotensive type 1 diabetic patients.

The reasons for the inconsistent association between salt consumption and blood pressure levels observed in within-society surveys are not known. A total of 157 normotensive subjects aged 18 to 35 years, selected at random in a cross-sectional population-based survey, answered a structured questionnaire. They were classified as strongly predisposed to hypertension when two or more first-degree relatives had a diagnosis of hypertension. Anthropometric parameters were obtained and sitting blood pressure was determined with aneroid sphygmomanometers. Sodium and potassium excretion was measured by flame spectrophotometry in an overnight urine sample. A positive correlation between blood pressure and urinary sodium excretion was detected only in the group of individuals strongly predisposed to hypertension, both for systolic blood pressure (r = 0.51, P<0.01) and diastolic blood pressure (r = 0.50, P<0.01). In a covariance analysis, after controlling for age, skin color and body mass index, individuals strongly predisposed to hypertension who excreted amounts of sodium above the median of the entire sample had higher systolic and diastolic blood pressure than subjects classified into the remaining conditions. The influence of familial predisposition to hypertension on the association between salt intake and blood pressure may be an additional explanation for the weak association between urinary sodium excretion and blood pressure observed in within-population studies, since it can influence the association between salt consumption and blood pressure in some but not all inhabitants.

Background: A positive association of chronic exposure to alcoholic beverages with blood pressure and the prevalence of hypertension has been described in epidemiological surveys, but the influence of time elapsed since last ingestion in this setting was not demonstrated., Design: A cross-sectional, population-based survey., Methods: In total 1089 adults from Porto Alegre, randomly selected from a population-based, multi-stage probability sample, were interviewed at home. The average daily alcohol intake of each subject was calculated taking into account the concentration of ethanol in the beverages (distilled or fermented beverages), and the time elapsed between the last ingestion of ethanol and the moment of blood pressure determination. Standardized sitting blood pressure and anthropometric parameters were collected. The magnitude and shape of the associations were analyzed considering blood pressure as a continuous variable and the prevalence of arbitrarily defined hypertension. Simple and multiple linear regression models, including models to identify nonlinear associations, with quadratic and cubic terms of the amount of alcohol consumed, were employed. Blood pressure means were compared by analysis of variance and analysis of covariance. The association between hypertension and exposure to ethanol was analyzed through logistic regression models, controlling for various potential confounders., Results: Positive nonlinear associations of the amount of alcohol consumed with blood pressure and the prevalence of hypertension (> or = 160/95 mmHg) were found, independent of age, years of education, smoking, and use of oral contraceptive and antihypertensive drugs. The consumption of 30 g/day ethanol was associated with increases of 1.5 and 2.3 mmHg in diastolic and systolic blood pressures, respectively, for men, and 2.1 and 3.2 mmHg, respectively, for women. The prevalence of hypertension was higher among those ingesting more than 30 g/day (odds ratio = 2.9, P < 0.01). The time elapsed between the last ingestion and blood pressure measurement was independently associated with the prevalence of hypertension. Men with last consumption of alcohol 13-23 h prior to measurement had odds of being hypertensive 2.6 (confidence interval 1.3-5.0) greater than did subjects who had consumed alcoholic beverages 24 h and more before the blood pressure determination. For men, systolic and diastolic blood pressures were lower during the first 3 h after ingestion and increased afterward. Frequency of consumption and type of beverage consumed were not independently associated with level of blood pressure., Conclusion: A time-dependent association between alcohol consumption and effects on blood pressure, demonstrated in experimental studies, was found for free-living individuals selected at random.

Autonomic neuropathy is a frequent complication of diabetes associated with higher morbidity and mortality in symptomatic patients, possibly because it affects autonomic regulation of the sinus node, reducing heart rate (HR) variability which predisposes to fatal arrhythmias. We evaluated the time course of arterial pressure and HR and indirectly of autonomic function (by evaluation of mean arterial pressure (MAP) variability) in rats (164.5 +/- 1.7 g) 7, 14, 30 and 120 days after streptozotocin (STZ) injection, treated with insulin, using measurements of arterial pressure, HR and MAP variability. HR variability was evaluated by the standard deviation of RR intervals (SDNN) and root mean square of successive difference of RR intervals (RMSSD). MAP variability was evaluated by the standard deviation of the mean of MAP and by 4 indices (P1, P2, P3 and MN) derived from the three-dimensional return map constructed by plotting MAPn x [(MAPn + 1)-(MAPn)] x density. The indices represent the maximum concentration of points (P1), the longitudinal axis (P2), and the transversal axis (P3) and MN represents P1 x P2 x P3 x 10(-3). STZ induced increased urinary glucose in diabetic (D) rats compared to controls (C). Seven days after STZ, diabetes reduced resting HR from 380.6 +/- 12.9 to 319.2 +/- 19.8 bpm, increased HR variability, as demonstrated by increased SDNN, from 11.77 +/- 1.67 to 19.87 +/- 2.60 ms, did not change MAP, and reduced P1 from 61.0 +/- 5.3 to 51.5 +/- 1.8 arbitrary units (AU), P2 from 41.3 +/- 0.3 to 29.0 +/- 1.8 AU, and MN from 171.1 +/- 30.2 to 77.2 +/- 9.6 AU of MAP. These indices, as well as HR and MAP, were similar for D and C animals 14, 30 and 120 days after STZ. Seven-day rats showed a negative correlation of urinary glucose with resting HR (r = -0.76, P = 0.03) as well as the MN index (r = -0.83, P = 0.01). We conclude that rats with short-term diabetes mellitus induced by STZ presented modified autonomic control of HR and MAP which was reversible. The metabolic control may influence these results, suggesting that insulin treatment and a better metabolic control in this model may modify arterial pressure, HR and MAP variability.

Background: The antihypertensive efficacy of drug therapy and of some nonpharmacologic recommendations has been demonstrated in controlled clinical trials, but not in a clinical setting., Objective: To assess the antihypertensive effectiveness of drug therapy and of three nonpharmacologic recommendations (loss of weight, salt-intake restriction, and physical exercise)., Design: A prospectively planned cohort study., Setting: A hospital-based hypertensive outpatient clinic., Patients: We studied 637 patients (65.5% women) with systolic blood pressures above 140 mmHg or diastolic blood pressures above 90 mmHg, corresponding to 76% of 839 patients who were administered a prescription for hypertension and who returned for the first follow-up visit 3.5 months later on average., Methods: The nonpharmacologic prescription consisted of salt-intake restriction for all, weight reduction for overweight patients, and practice of aerobic physical exercise for those for whom it was not contraindicated; 60% of the patients were treated with drugs according to standard recommendations. Patients treated with drugs were compared with untreated subjects; for the nonpharmacologic interventions, the groups were compared according to their reported compliances with the recommendations (at least some compliance versus none). The main outcome measures were variations in systolic and diastolic blood pressures between the baseline evaluation and the first follow-up visit and an improvement in prognosis, represented by a favorable change in the classification of the blood pressure (according to Joint National Committee V criteria)., Results: The cohort constituted predominantly low-income, middle-aged, overweight white women, with low-to-moderate hypertension of long duration. The group treated with drugs exhibited the greatest reduction in blood pressure, with clinical significance even discounting the losses in follow-up; the group of patients who reported compliance with the low-energy-intake diet also showed a consistent antihypertensive effect, which was still detectable on the occasion of the third follow-up visit 9 months after the first prescription; reported compliance with a low-sodium diet and practice of physical exercise were not associated with a reduction in blood pressure; among a subset of the patients, reported compliance with the salt-intake-restricted diet did not reduce the amount of sodium to the theoretical antihypertensive threshold. It was not possible to determine whether the lack of an antihypertensive effect of physical exercise for this cohort was secondary to a misreport of the extent of compliance or to an absence of effect of the intensity of training prescribed. The effects of drug therapy and compliance with a low-energy-intake diet were shown to be independent of other interventions or confounders., Conclusion: The antihypertensive effect of drugs demonstrated in well-controlled clinical trials is achievable in clinical practice. The recommendation to lose weight was the only nonpharmacologic intervention with a detectable antihypertensive effect in this cohort. The absence of effect of a low-sodium diet is probably secondary to the insufficient reduction in the amount of salt consumed. The lack of an antihypertensive effect of physical exercise could reflect either a misreported compliance or an absence of effect of the intensity of training recommended in this study.