Post-resistance exercise hemodynamic and autonomic responses: Comparison between normotensive and hypertensive men.

To compare post-resistance exercise hypotension (PREH) and its mechanisms in normotensive and hypertensive individuals, 14 normotensives and 12 hypertensives underwent two experimental sessions: control (rest) and exercise (seven exercises, three sets, 50% of one repetition maximum). Hemodynamic and autonomic clinic measurements were taken before (Pre) and at two moments post-interventions (Post 1: between 30 and 60 min; Post 2: after 7 h). Ambulatory blood pressure (BP) was monitored for 24 h. At Post 1, exercise decreased systolic BP similarly in normotensives and hypertensives (-8 ± 2 vs -13 ± 2 mmHg, P > 0.05), whereas diastolic BP decreased more in hypertensives (-4 ± 1 vs -9 ± 1 mmHg, P < 0.05). Cardiac output and systemic vascular resistance did not change in normotensives and hypertensives (0.0 ± 0.3 vs 0.0 ± 0.3 L/min; -1 ± 1 vs -2 ± 2 U, P > 0.05). After exercise, heart rate (+13 ± 3 vs +13 ± 2 bpm) and its variability (low- to high-frequency components ratio, 1.9 ± 0.4 vs +1.4 ± 0.3) increased whereas stroke volume (-14 ± 5 vs -11 ± 5 mL) decreased similarly in normotensives and hypertensives (all, P > 0.05). At Post 2, all variables returned to pre-intervention, and ambulatory data were similar between sessions. Thus, a session of resistance exercise promoted PREH in normotensives and hypertensives. Although this PREH was greater in hypertensives, it did not last during the ambulatory period, which limits its clinical relevance. In addition, the mechanisms of PREH were similar in hypertensives and normotensives.

Amlodipine reduces blood pressure during dynamic resistance exercise in hypertensive patients.

This study investigated the effect of the dihydropyridine calcium channel antagonist, amlodipine, on blood pressure (BP) during resistance exercise performed at different intensities in hypertensives. Eleven hypertensives underwent 4 weeks of placebo and amlodipine (random double-blinded crossover design). In each phase, they performed knee extension exercise until exhaustion following three protocols: one set at 100% of 1 RM (repetition maximum), three sets at 80% of 1 RM, and three sets at 40% of 1 RM. Intraarterial BP was measured before and during exercise. Amlodipine reduced maximal systolic/diastolic BP values achieved at all intensities (100% = 225 ± 6/141 ± 3 vs. 207 ± 6/130 ± 6 mmHg; 80% = 289 ± 8/178 ± 5 vs. 273 ± 10/169 ± 6 mmHg; 40% = 289 ± 10/176 ± 8 vs. 271 ± 11/154 ± 6 mmHg). Amlodipine blunted the increase in diastolic BP that occurred during the second and third sets of exercise at 40% of 1RM (+75 ± 6 vs. +61 ± 5 mmHg and +78 ± 7 vs. +64 ± 5 mmHg, respectively). Amlodipine was effective in reducing the absolute values of systolic and diastolic BP during resistance exercise and in preventing the progressive increase in diastolic BP that occurs over sets of low-intensity exercise. These results suggest that systemic vascular resistance is involved in BP increase during resistance exercise, and imply that hypertensives receiving amlodipine are at lower risk of increased BP during resistance exercise than non-medicated patients.

Presence of Campylobacter and Arcobacter species in in-line milk filters of farms authorized to produce and sell raw milk and of a water buffalo dairy farm in Italy.

The objectives of this study were to investigate the presence of Campylobacter spp. and Arcobacter spp. in dairy herds authorized for the production and sale of raw milk and in a water buffalo dairy farm, and to test the antimicrobial susceptibility of the isolates. A total of 196 in-line milk filters were collected from 14 dairy farms (13 bovine and 1 water buffalo) for detection of Campylobacter spp. and Arcobacter spp. by microbiological culture. For each farm investigated, 1 isolate for each Campylobacter and Arcobacter species isolated was tested using the Etest method (AB Biodisk, Solna, Sweden) to evaluate the susceptibility to ciprofloxacin, tetracycline, chloramphenicol, ampicillin, erythromycin, and gentamicin. A total of 52 isolates were detected in 49 milk filters in 12 farms (85.7%) out of 14 and the isolates were identified as Campylobacter jejuni (6), Campylobacter hyointestinalis ssp. hyointestinalis (8), Campylobacter concisus (1), Campylobacter fetus ssp. fetus (1), Arcobacter butzleri (22), and Arcobacter cryaerophilus (14). The small number of isolates tested for antimicrobial susceptibility precludes any epidemiological consideration but highlights that all Campylobacter isolates were susceptible to macrolides, which are the first-choice drugs for the treatment of campylobacteriosis, and that resistance to fluoroquinolones and tetracycline was detected; for Arcobacter isolates, resistance to ampicillin and chloramphenicol was detected. The sale of raw milk for human consumption by self-service automatic vending machines has been allowed in Italy since 2004 and the presence of C. jejuni in in-line milk filters confirms that raw milk consumption is a significant risk factor for human infection. The high occurrence of emerging Campylobacter spp. and Arcobacter spp. discovered in dairy farms authorized for production and sale of raw milk represents an emerging hazard for human health.

Gender influence on post-resistance exercise hypotension and hemodynamics.

Post-resistance exercise hypotension has been extensively described in men and women. However, gender influence on this response has not yet been clear. Gender might change post-exercise hemodynamics, since men and women respond differently during exercise. Thus, the purpose was to compare post-resistance exercise hypotension and its hemodynamic determinants in men and women. Normotensive subjects (22-male, 22-female) underwent 2 sessions: control (40 min of rest) and exercise (6 resistance exercises, 3 sets, 20 repetitions, at 40-50% of 1RM). Blood pressure, heart rate, and cardiac output were measured prior to and following interventions. Blood pressure decrease after exercise was similar between the genders. However, hemodynamic determinants responded differently in men and women. Systemic vascular resistance reduced in women (-4.6±1.9U, P<0.05), while cardiac output decreased in men (-0.6±0.2 L/min, P<0.05). This response was accompanied by a decrease in stroke volume in men (-21.6±5.1 ml, P<0.05) and a more pronounced increase in heart rate in men than in women (+11.3±1.3 vs. +6.5±1.7 bpm, P<0.05, respectively). In conclusion, post-resistance exercise hypotension was similar in men and women. However, its hemodynamic determinants differ between the genders, depending on cardiac output decrease in men and on systemic vascular resistance decrease in women.

Finger blood pressure during leg resistance exercise.

Blood pressure (BP) assessment during resistance exercise can be useful to avoid high BP, reducing cardiovascular risk, especially in hypertensive individuals. However, non-invasive accurate technique for this purpose is not available. The aim of this study was to compare finger photoplethysmographic (FPP) and intra-arterial BP values and responses during resistance exercise. Eight non-medicated hypertensive subjects (5 males, 30-60 years) were evaluated during pre-exercise resting period and during three sets of the knee extension exercise performed at 80% of 1RM until fatigue. BP was measured simultaneously by FPP and intra-arterial methods. Data are mean+/-SD. Systolic BP was significantly higher with FPP than with intra-arterial: at pre-exercise (157+/-13 vs. 152+/-10 mmHg; p<0.01) and the mean (202+/-29 vs. 198+/-26 mmHg; p<0.01), and the maximal (240+/-26 vs. 234+/-16 mmHg; p<0.05) values achieved during exercise. The increase in systolic BP during resistance exercise was similar between FPP and intra-arterial (+73+/-29 vs. +71+/-18 mmHg; p=0.59). Diastolic BP values and increases were lower with FPP. In conclusion, FPP provides similar values of BP increment during resistance exercise than intra-arterial method. However, it overestimates by 2.6+/-6.1% the maximal systolic BP achieved during this mode of exercise and underestimates by 8.8+/-5.8% the maximal diastolic BP.

Validity of four indirect methods to measure adherence in primary care hypertensives.

High blood pressure (HBP) is one of the most important risk factors for morbidity and mortality in the world. Non-adherence to medication is associated with the lack of control of HBP. The objective of this study was to assess the validity of four indirect methods for measuring adherence to medication to control HBP in primary health care. A random sample of 120 hypertensive patients who were undergoing treatment for at least 2 months in a primary care unit in Florianópolis (Brazil) were included in the study. The independent variables were four indirect methods to measure adherence to medication: knowledge regarding the HBP medication, the blood pressure level, attitude regarding the medication intake (Morisky-Green test) and self-reported adherence. The classification of HBP was based on criteria established by the Brazilian Ministry of Health. The gold standard used for measuring adherence was the pill count. Logistic regression was used to estimate sensitivity (highest value of 88.2% for self-report), specificity (highest value of 70.7% for HBP control), positive predictive value (highest value of 46.4% for HBP control) and negative predictive value (highest value of 79.1% for Morisky-Green test) for each of the indirect methods. No indirect method of measuring adherence had a good positive predictive value for adherence, which was best predicted by patients' age and whether they managed to control HBP. The results also revealed low treatment adherence (31.2%) and low control of HBP (37.6%). Non-adherence was mainly associated with side effects of the treatment.

Antihypertensive efficacy of amlodipine and losartan after two 'missed' doses in patients with mild to moderate essential hypertension.

We compared the effects of amlodipine (5-10 mg, n=94) and losartan (50-100 mg, n=94) on the lowering of blood pressure (BP) at steady state and after two missed doses, as well as on tolerability. This was a randomized, double-blind study of 12 weeks of active treatment followed by 2 days of placebo treatment. Twenty-four-hour ambulatory blood pressure monitoring and office BP measurements were performed at baseline, week 12 and after the 2-day drug holiday. After 12 weeks, amlodipine was significantly more effective than losartan in reducing both 24-h systolic blood pressure (SBP) (-18.0 versus -10.8 mmHg) and diastolic blood pressure (DBP) (-10.6 versus -8.0 mmHg). While mean SBP and DBP for both treatments increased comparably during the drug holiday, BP values remained significantly lower than baseline for both treatments. The superior BP-lowering effect of amlodipine compared with losartan was maintained during the drug holiday.

Previous exercise attenuates muscle sympathetic activity and increases blood flow during acute euglycemic hyperinsulinemia.

Insulin infusion causes muscle vasodilation, despite the increase in sympathetic nerve activity. In contrast, a single bout of exercise decreases sympathetic activity and increases muscle blood flow during the postexercise period. We tested the hypothesis that muscle sympathetic activity would be lower and muscle vasodilation would be higher during hyperinsulinemia performed after a single bout of dynamic exercise. Twenty-one healthy young men randomly underwent two hyperinsulinemic euglycemic clamps performed after 45 min of seated rest (control) or bicycle exercise (50% of peak oxygen uptake). Muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (FBF, plethysmography), blood pressure (BP, oscillometric method), and heart rate (HR, ECG) were measured at baseline (90 min after exercise or seated rest) and during hyperinsulinemic euglycemic clamps. Baseline glucose and insulin concentrations were similar in the exercise and control sessions. Insulin sensitivity was unchanged by previous exercise. During the clamp, insulin levels increased similarly in both sessions. As expected, insulin infusion increased MSNA, FBF, BP, and HR in both sessions (23 +/- 1 vs. 36 +/- 2 bursts/min, 1.8 +/- 0.1 vs. 2.2 +/- 0.2 ml.min(-1).100 ml(-1), 89 +/- 2 vs. 92 +/- 2 mmHg, and 58 +/- 1 vs. 62 +/- 1 beats/min, respectively, P < 0.05). BP and HR were similar between sessions. However, MSNA was significantly lower (27 +/- 2 vs. 31 +/- 2 bursts/min), and FBF was significantly higher (2.2 +/- 0.2 vs. 1.8 +/- 0.1 ml.min(-1).100 ml(-1), P < 0.05) in the exercise session compared with the control session. In conclusion, in healthy men, a prolonged bout of dynamic exercise decreases MSNA and increases FBF. These effects persist during acute hyperinsulinemia performed after exercise.

Effects of alcohol on sympathetic activity, hemodynamics, and chemoreflex sensitivity.

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.

Effects of fludrocortisone on sympathetic nerve activity in humans.

Fludrocortisone reduces plasma norepinephrine in healthy humans, but forearm vascular and pressor responses to norepinephrine are potentiated. The effects of fludrocortisone on sympathetic nerve activity in healthy humans are not known. To investigate these effects we evaluated muscle sympathetic nerve activity, heart rate, and arterial pressure in 11 healthy volunteers during three protocols: (1) before and on day 7 of fludrocortisone (0.4 mg/d) treatment with ad libitum diet (n = 6); (2) before and on day 7 of fludrocortisone (0.4 mg/d) or placebo with a 150 mmol/24 h (mEq/24 h) sodium diet (n = 7); and (3) before and on day 2 of fludrocortisone (0.4 mg/d) or placebo with a 150 mmol/24 h (mEq/24 h) sodium diet (n = 4). Placebo did not alter any parameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreflex control of muscle sympathetic nerve activity in mild hypertension.

The importance of the arterial baroreflex control of muscle sympathetic nerve activity (MSNA) has been investigated in physiological conditions and in cardiovascular dysfunctions. However, there is no consensus about the role played by the MSNA in hypertensive states, probably due to the diversity of the methods used to study the arterial baroreflex control of MSNA. In the present study we evaluated the reflex changes in MSNA by increasing and decreasing the mean arterial pressure (MAP) through 1 min intravenous infusion of phenylephrine (1 microgram/kg) and sodium nitroprusside (1 microgram/kg), respectively, in eight normotensive and eight mild hypertensive subjects. Both MAP and MSNA were significantly higher in hypertensive (117 +/- 2 mm Hg and 30 +/- 3 bursts/min) than in normotensive (96 +/- 4 mm Hg and 20 +/- 3 bursts/min) subjects. The reflex gain was calculated by the ratio percent of changes in MSNA/percent changes in MAP. The maximal reflex gain was statistically similar in normotensive and hypertensive groups during phenylephrine (5.1 +/- .4 v 4.3 +/- 0.4 bursts/mm Hg, respectively) and nitroprusside (10.7 +/- 2.3 v 8.1 +/- 1.3 bursts/mm Hg, respectively) infusion. The present data showing that arterial baroreflex control of MSNA is not depressed in hypertensive subjects indicate that the elevated basal MSNA and the mild hypertension in human beings is not a consequence of baroreflex control of MSNA dysfunction.

Postexercise responses of muscle sympathetic nerve activity and blood flow to hyperinsulinemia in humans.

Although insulin and exercise cause dramatic changes in physiological parameters, the impact of exercise on neural and hemodynamic responses to insulin administration has not been described. In a study of the effects of a single bout of exercise on blood pressure (BP), muscle sympathetic nerve activity (MSNA), and forearm blood flow (FBF) responses to insulin infusion during the postexercise period, 11 healthy men underwent, in a random order, two hyperinsulinemic euglycemic clamps performed after 45 min of 1) bicycle exercise (50% peak O(2) uptake, Exercise session) and 2) seated rest (Control session). Data were analyzed during baseline and steady-state periods. Although insulin levels and insulin sensitivity were similar, baseline plasma glucose levels were significantly lower in the Exercise than in the Control session. Mean BP was significantly lower (3%) and FBF was higher (27%) in the Exercise session. Exercise increased insulin-induced MSNA enhancement (84%) without changing FBF and BP responses to hyperinsulinemia. In conclusion, a single bout of exercise that does not alter insulin sensitivity exacerbates insulin-induced increase in MSNA without changing FBF and BP responses to hyperinsulinemia.

How accurate are sphygmomanometers?

The objective of this study was to assess the accuracy and reliability of mercury and aneroid sphygmomanometers. Measurement of accuracy of calibration and evaluation of physical conditions were carried out in 524 sphygmomanometers, 351 from a hospital setting, and 173 from private medical offices. Mercury sphygmomanometers were considered inaccurate if the meniscus was not '0' at rest. Aneroid sphygmomanometers were tested against a properly calibrated mercury manometer, and were considered calibrated when the error was < or =3 mm Hg. Both types of sphygmomanometers were evaluated for conditions of cuff/bladder, bulb, pump and valve. Of the mercury sphygmomanometers tested 21 % were found to be inaccurate. Of this group, unreliability was noted due to: excessive bouncing (14%), illegibility of the gauge (7%), blockage of the filter (6%), and lack of mercury in the reservoir (3%). Bladder damage was noted in 10% of the hospital devices and in 6% of private medical practices. Rubber aging occurred in 34% and 25%, leaks/holes in 19% and 18%, and leaks in the pump bulb in 16% and 30% of hospital devices and private practice devices, respectively. Of the aneroid sphygmomanometers tested, 44% in the hospital setting and 61% in private medical practices were found to be inaccurate. Of these, the magnitude of inaccuracy was 4-6 mm Hg in 32%, 7-12 mm Hg in 19% and > 13 mm Hg in 7%. In summary, most of the mercury and aneroid sphygmomanometers showed inaccuracy (21% vs 58%) and unreliability (64% vs 70%).

Salt supresses baseline muscle sympathetic nerve activity in salt-sensitive and salt-resistant hypertensives.

The objective of our study was to evaluate the role of the baroreflex control of peripheral sympathetic nervous system on the increase of muscle sympathetic nerve activity (MSNA) in salt-sensitive (SS) and salt-resistant (SR) hypertensives under low salt diet. In phase I mild-to-moderate hypertensive patients (n=5) received three diet periods: a first regular salt (RS1), a low salt (LS=20 meq Na+/day), followed by a second regular salt diet (RS2) with a 7-day duration of each. At the end of each period, sympathetic and heart rate baroreflex control were recorded. Baseline MSNA varied (P<0.005) from 18+/-8 (RS1) to 32+/-9 (LS) and to 14+/-9 (RS2) bursts per minute (bpm). In phase II additional patients (n=6) were included to have baseline MSNA, sympathetic and heart rate baroreflex control evaluated at the end of the LS and RS2. For all patients (n=11), there was a significant decrease of MSNA from 36+/-4 to 20+/-8 bpm on day 7 of LS to RS2 (P<0.05). The response of MSNA to a salt restriction was similar for SS and SR patients, who showed a change from 32+/-6 to 18+/-11 and from 36+/-9 to 17+/-7 bpm for SS and SR on day 7 of LS and RS2 diets, respectively (P<0.05). MSNA baroreflex gain was similar during phenylephrine infusions at day 7 of LS and RS2 (5.1+/-1.6 and 6.1+/-2.9 bpm/mmHg), but it was reduced under LS during sodium nitroprusside infusion (19.5+/-4.9 vs 8.9+/-0.7 bpm/mmHg) (P<0.05) for the whole group. Baroreflex control of MSNA was also similar during phenylephrine infusions under LS and RS2 diets for SS (4.0+/-0.9 and 3.3+/-0.2 bpm/mmHg) and for SR patients (10.1+/-2.5 and 5.6+/-1.5 bpm/mmHg). During nitroprusside infusion, baroreflex gain was significantly greater under RS2 for SR patients (19.5+/-2.6 bpm/mmHg) when compared to LS (11.2+/-5.2 bpm/mmHg) and the same significant difference was observed among SS patients (14.4+/-4.7 and 9.1+/-3.6 bpm/mmHg under RS2 and LS diets, respectively). There was no difference in heart rate baroreflex gain between LS and RS2 diets. Data support the hypotheses that (1) sodium supresses baseline MSNA in SS and SR hypertensives and (2) sodium restriction may impair baroreflex control of MSNA in SR and SS mild-to-moderate hypertensive patients during blood pressure reductions.

Mild chronic renal insufficiency induces sympathetic overactivity.

The objectives of this study were to evaluate baseline sympathetic nerve activity as well as the mechanisms of sympathetic overactivity in mild chronic renal insufficiency hypertension. Seven hypertensives with mild renal insufficiency, seven hypertensives with normal renal function and seven normotensives, age and weight-matched were studied on one session to evaluate baseline muscle sympathetic nerve activity measured in the peroneal nerve. The mild renal insufficiency hypertensives and the hypertensives with normal renal function were also studied to evaluate arterial baroreflex control of muscle sympathetic nerve activity assessed by increasing and decreasing blood pressure through continuous infusion of phenylephrine and sodium nitroprusside respectively. Baseline muscle sympathetic nerve activity was significantly higher in mild renal insufficiency hypertensives (34 bursts/min) when compared to hypertensives with normal renal function (24 bursts/min) and to normotensives (16 bursts/min). Baroreflex control of muscle sympathetic nerve activity was (in absolute values) 15.2 in hypertensives with normal renal function vs 2.6 in mild renal insufficiency hypertensives (P < 0.05) during phenylephrine and 6.3 vs 8.2 during nitroprusside infusions. Mild renal insufficiency hypertensives showed sympathetic overactivity when compared to hypertensives with normal renal function and to normotensives. This finding demonstrates that elevated sympathetic activity may be precociously detected in renal insufficiency. Baroreflex gain to phenylephrine was blunted in mild renal insufficiency hypertensives when compared to hypertensives with normal renal function, suggesting that bradycardic response in mild renal insufficiency is blunted.

The addition of mibefradil to chronic hydrochlorothiazide therapy in hypertensive patients is associated with a significant antihypertensive effect.

OBJECTIVE: To evaluate the antihypertensive efficacy, tolerability, safety, and dose-response characteristics of the novel calcium antagonist, mibefradil, in combination with a diuretic regimen. DESIGN: A multinational, double-blind, randomised, placebo-controlled, parallel-design trial. METHODS: Three hundred and seven patients whose mild-to-moderate essential hypertension remained uncontrolled after 4 weeks of treatment with hydrochlorothiazide (HCTZ) 25 mg/day and placebo were randomised to receive combined treatment with HCTZ and once-daily doses of 12.5, 25, 50, or 100 mg of mibefradil or placebo. After 8 weeks of combined treatment, HCTZ was withdrawn and the mibefradil groups continued on their respective doses for an additional 6 weeks. RESULTS: After 8 weeks, the addition of once-daily doses of mibefradil to the initial HCTZ regimen resulted in clinically relevant, dose-related reductions in sitting diastolic blood pressure (SDBP) and sitting systolic blood pressure (SSBP) at trough, which were significantly greater in the 50 and 100 mg dose groups compared to the placebo group (P < or = 0.003). Placebo-corrected treatment effects on SDBP and SSBP at the end of the combined treatment period relative to baseline were, respectively, -4.1 and -8.0 mm Hg in the 50 mg mibefradil group and -9.5 and -8.0 mm Hg in the 100 mg mibefradil group. Therapeutic response rates to combination mibefradil and HCTZ therapy were high and dose related, reaching 82% for SDBP in the 100 mg group. CONCLUSIONS: The addition of once-daily doses of 50 or 100 mg of mibefradil to patients whose hypertension is not controlled by HCTZ alone is well tolerated and effective in improving BP control.

Factors affecting post-exercise hypotension in normotensive and hypertensive humans.

BACKGROUND: Post-exercise hypotension has been extensively described under laboratory conditions. However, studies investigating the persistence of this post-exercise decrease in blood pressure for longer periods have produced controversial results. The present investigation was conducted to verify the effect of a single bout of exercise on ambulatory blood pressure and to identify potential factors that might influence this post-exercise ambulatory blood pressure fall. DESIGN: The study was a randomized controlled clinical trial. METHODS: Thirty normotensive and 23 hypertensive subjects were submitted to two ambulatory blood pressure monitorings (using the SpaceLabs 90207, SpaceLabs, Redmond, Washington, USA), which were performed after 45min of seated rest (control session) or cycling exercise at 50% peak oxygen uptake (exercise session). RESULTS: Normotensive subjects demonstrated a lower 24h blood pressure level in the exercise session. Hypertensive patients showed no significant difference in ambulatory blood pressure level between the two experimental sessions. Further data analysis revealed that approximately 65% of the subjects in both groups experienced a fall in blood pressure after exercise. Moreover, in the normotensive subjects, this blood pressure fall was significantly and positively correlated with clinic and ambulatory blood pressure, and negatively correlated with weight and body mass index. The blood pressure response to exercise was also greater in women. In the hypertensive patients, the post-exercise blood pressure decrease was significantly and positively correlated with clinic and ambulatory blood pressure as well as with the peak oxygen uptake, and negatively correlated with age and body mass index. CONCLUSIONS: The post-exercise ambulatory blood pressure fall observed in normotensive and hypertensive humans depends on individual characteristics. Moreover, in both normotensive and hypertensive humans, post-exercise ambulatory hypotension is greater in subjects with a higher initial blood pressure level.

Population studies of ambulatory blood pressure monitoring in Brazilian children.

BACKGROUND: The determination of hypertension in a given population depends on the knowledge of population norms for blood pressure. This is true for both casual blood pressure (CBP) measurements and the newest and most promising technology of ambulatory blood pressure monitoring (ABPM). OBJECTIVE: To design an ambitious multinational co-operative study to determine normal blood pressure data in Brazilian children. METHODS: The study was designed to determine normative data for CBP, using the Task Force technical recommendations for age-, sex- and height-percentile-specific blood pressure values. The proposed procedure is as follows. ABPM will be studied in a random subgroup of individuals, to develop similar normative data. These data will be correlated to CBP measurements and to echocardiographic findings as a measure of end-organ damage. All patients who are diagnosed by CBP measurement to be hypertensive will also be studied by ABPM, and studies of target-organ damage will be performed. Family and medical histories will be evaluated by questionnaire and first-degree relatives will be evaluated for CBP measurement. Hypertensive patients will form a cohort for long-term follow-up. These data will be the foundation for studies of hypertension in Brazilian children.

The international database of self-recorded blood pressures in normotensive and untreated hypertensive subjects.

OBJECTIVES: To pool data from individual subjects in an attempt to determine an operational threshold for making clinical decisions based on the self-recorded blood pressure (SRBP) and to examine how many hypertensive subjects, diagnosed by conventional blood pressure (CBP) measurement, would have a self-recorded blood pressure within the normotensive range if the proposed thresholds were applied. DATA SOURCES: Thirteen research groups studied 4668 untreated subjects. RESULTS: In total 2401 subjects were normotensive, 494 were borderline hypertensive and 1773 were definitely hypertensive. Hypertension had been diagnosed from the mean of 1-6 (median 3) CBP measurements obtained during 1-3 (median 1) visits. The reference values for SRBP measurements determined from the 95th percentiles of the distributions for normotensive subjects were 137 mmHg systolic and 85 mmHg diastolic. Of the subjects with systolic hypertension, 16% had systolic SRBP

The effect of siesta in parameters of cardiac structure and in interpretation of ambulatory arterial blood pressure monitoring.

OBJECTIVE: To evaluate the influence of the siesta in ambulatory blood pressure (BP) monitoring and in cardiac structure parameters. METHODS: 1940 ambulatory arterial blood pressure monitoring tests were analyzed (Spacelabs 90207, 15/15 minutes from 7:00 to 22:00 hours and 20/20 minutes from 22:01 to 6.59hours) and 21% of the records indicated that the person had taken a siesta (263 woman, 52+/-14 years). The average duration of the siesta was 118+/-58 minutes. RESULTS: (average +/- standard deviation) The average of systolic/diastolic pressures during wakefulness, including the napping period, was less than the average for the period not including the siesta (138+/-16/85+/-11 vs 139+/-16/86+/-11 mmHg, p<0. 05); 2) pressure loads during wakefulness including the siesta, were less than those observed without the siesta); 3) the averages of nocturnal sleep blood pressures were similar to those of the siesta, 4) nocturnal sleep pressure drops were similar to those in the siesta including wakefulness with and without the siesta; 5) the averages of BP in men were higher (p<0.05) during wakefulness with and without the siesta, during the siesta and nocturnal sleep in relation to the average obtained in women; 6) patients with a reduction of 0- 5% during the siesta had thickening of the interventricular septum and a larger posterior wall than those with a reduction during the siesta >5%. CONCLUSION: The siesta influenced the heart structure parameters and from a statistical point of view the average of systolic and diastolic pressures and the respective pressure loads of the wakeful period.