Exercise In Hypertensive Patients Research Articles

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.

The association of left ventricular hypertrophy (LVH) with intraventricular dyssynchrony at rest and during exercise in hypertensive patients

The association of left ventricular hypertrophy (LVH) with intraventricular dyssynchrony at rest and during exercise in hypertensive patients

Inhibition of the renin–angiotensin system does not reduce platelet activity at rest or during stress in hypertension

We investigated the influence of angiotensin receptor blockade and angiotensin-converting enzyme inhibition on stress-induced platelet activation in hypertensive patients. Secondary aims were effects on inflammation, coagulation, and endothelial function. Following a 4-week placebo period, 25 hypertensive patients entered a double-blind, crossover study comparing enalapril (20 mg once daily) and losartan (100 mg once daily) treatment (each for 8 weeks). Patients were studied at rest and after a standardized exercise test. Mean arterial pressure was reduced from 119 ± 2 to 104 ± 2 (enalapril) and 106 ± 2 (losartan) mmHg (both P <0.001). Plasma angiotensin II decreased from 2.4 ± 0.4 to 0.5 ± 0.1 pmol/l with enalapril, and increased to 7.2 ± 1.3 pmol/l with losartan (both P <0.001). Exercise-evoked platelet activation, as evidenced by increased numbers of P-selectin-positive platelets (P <0.01), elevated circulating platelet-platelet aggregates (P <0.01) and soluble P-selectin levels (P <0.001), and increased platelet responsiveness to adenosine diphosphate and thrombin (both P <0.05). Neither drug influenced these markers of platelet activation at rest or following exercise. Markers of inflammation (high-sensitivity C reactive protein, interleukin-6, tissue necrosis factor-α), coagulation (tissue plasminogen activator antigen, prothrombin fragment F1+2), and endothelial function (von Willebrand factor, soluble vascular cellular adhesion molecule-1, and intercellular adhesion molecule-1) were also uninfluenced by treatment. Enalapril and losartan failed to reduce platelet activity both at rest and during exercise in hypertensive patients. Markers of inflammation, coagulation, and endothelial function were similarly unaffected. Inhibition of the renin-angiotensin system promotes its beneficial effects in hypertension through mechanisms other than platelet inhibition.

The Changes of Noninvasive Hemodynamic Parameters after Device-Guided Slow Breathing Exercise in Hypertensive Patients

The Changes of Noninvasive Hemodynamic Parameters after Device-Guided Slow Breathing Exercise in Hypertensive Patients

474 AMLODIPINE DECREASES BLOOD PRESSURE LEVELS DURING RESISTANCE EXERCISE IN HYPERTENSIVE SUBJECTS.

Objective: Dynamic resistance exercise is recommended for hypertensives. However, blood pressure (BP) increases substantially during its execution due, in part, to peripheral vascular resistance increase. Calcium channel antagonists are commonly used for decreasing peripheral resistance, and consequently BP. This study was designed to test if amlodipine (5 mg) was able to decrease BP absolute levels and BP increase during dynamic resistance exercise performed at low intensity in subjects hypertensives. Design and Methods: The study had a double-blinded cross-over design. Nine 9 essential hypertensives (systolic-SBP/diastolic-DBP between 140/90 and 160/105 mmHg) underwent, in a random order, 4 weeks of placebo and amlodipine treatment, preceded by 2 weeks of any drug washout. At the 4th week of each treatment, the volunteers executed 3 sets of the knee extension exercise to fatigue at 40% of 1RM, with a 90-s rest interval between the sets. Intra-arterial radial BP and heart rate (HR) were measured throughout the protocols. Data was compared by 2-way ANOVA for repeated measures.Conclusion: In conclusion, amlodipine reduced SBP and DBP absolute values achieved during resistance exercise, but didn’t change BP increase during this kind of exercise in hypertensive patients. Financial Support: FAPESP (2009/12572-3) Medication Donation: Medley

A Vasodilating β1 Blocker Celiprolol Inhibits Muscular Release of Uric Acid Precursor in Patients with Essential Hypertension

Although nonvasodilating β1 blockers increase the levels of uric acid in serum, it is not known whether vasodilating β1 blockers have a similar effect. In the present study, we evaluated the effect of celiprolol on the release of hypoxanthine, a uric acid precursor, from muscles after an exercise. We used the semi-ischemic forearm test to examine the release of lactate (ΔLAC), ammonia (ΔAmm), and hypoxanthine (ΔHX) before and 4, 10, and 60 min after an exercise in 18 hypertensive patients as well as 4 normotensive subjects. Before celiprolol treatment, all the levels of ΔHX and ΔAmm, and ΔLAC were increased by semi-ischemic exercise in hypertensive patients, and the increases were remarkably larger than those in normotensive subjects. Celiprolol decreased both systolic and diastolic pressure. It also decreased the levels of ΔHX and ΔAmm without changes in ΔLAC after an exercise. These findings also were confirmed by summation of each metabolite (ΣΔMetabolites). Celiprolol caused a marginal decrease of serum uric acid, but the difference was not statistically significant. On the other hand, nonvasodilating β1 blockers did not suppress the levels of ΔHX and ΔAmm, whereas they significantly increased ΔLAC after an exercise. Celiprolol improved energy metabolism in skeletal muscles. It suppressed HX production and consequently did not adversely affect serum uric acid levels.

The Association of Left Ventricular Hypertrophy with Intraventricular Dyssynchrony at Rest and during Exercise in Hypertensive Patients

BackgroundImpaired exercise tolerance with dyspnea is common in hypertensive patients and this may be due to the exaggeration of nonuniform ventricular activation during exercise. So we want to evaluate the effect of left ventricular hypertrophy (LVH) on systolic intraventricular dyssynchrony during exercise.MethodsA total of 85 patients with hypertension who having exertional dyspnea and 30 control individuals were enrolled. Exercise stress echocardiography was performed using a symptom limited, multistage supine bicycle test. To evaluate the dyssynchrony of left ventricular (LV), we calculated the standard deviation (SD) of the averaged time-to-peak systolic velocity (TPs-SD, ms) of 12 middle and basal LV segments obtained from the three standard apical views at rest and peak exercise.ResultsThere was no significant difference in systolic blood pressure (BP) and heart rate between the two groups. TPs-SD was significantly higher in patients with LVH at rest (31.5 ± 12.1 vs. 22.0 ± 12.6 ms, p = 0.002) with exaggeration of the degree at peak exercise (39.0 ± 11.9 vs. 24.6 ± 13.3 ms, p < 0.001). Multiple regression analysis showed LV mass index was independently associated with LV dyssynchrony at peak exercise (β = 0.515, p = 0.001) when controlled for age, sex, and systolic BP at peak exercise.ConclusionIntraventricular systolic dyssynchrony during exercise is significantly associated with the degree of LVH in hypertensive patients.

The Effect of Metabolic Syndrome on Myocardial Contractile Reserve during Exercise in Non-Diabetic Hypertensive Subjects

BackgroundMetabolic syndrome (MS) is associated with increased left ventricular (LV) mass and diastolic dysfunction. This study uses relatively load-independent Doppler tissue echocardiography to examine whether MS is associated with decreased longitudinal contractile reserve during dynamic exercise.MethodsA total of 112 patients with relatively well-controlled, treated hypertension who complained of exertional dyspnea were enrolled (average age: 56.7 ± 10.5 years). Fifty-six were non-diabetic patients with MS (Group 1), and 56 were age-sex matched hypertensive patients without MS (Group 2). Exercise stress echo was performed using a symptom-limited, multistage, supine bicycle exercise test. Multiple Doppler parameters were obtained at baseline, at each stage of exercise, and during recovery.ResultsThere was no significant difference between the two groups in terms of age, gender, and hemodynamic variables. E/E', an index of LV filling pressure, was significantly higher in the MS group at rest and during exercise. The longitudinal contractile reserve, the change in S' (longitudinal tissue velocity) from baseline to peak exercise, was significantly lower in the MS group (2.00 ± 1.65 vs. 2.90 ± 1.66, p = 0.015). Multiple regression analysis showed independent association of MS with longitudinal contractile reserve when controlled for confounding factors, such as LV mass index, gender, blood pressure, and age (β = -0.235, p = 0.035).ConclusionLongitudinal contractile reserve was reduced in MS patients compared to others, although both groups demonstrated similar longitudinal contractile function at rest. We present the first demonstration that metabolic syndrome is independently associated with LV systolic dysfunction during exercise in hypertensive patients.

Exercise in hypertension: do skeletal muscle reflexes make this a dangerous proposition?

the benefits of exercise and exercise training are numerous, varying from increasing skeletal muscle strength to enhancing cardiovascular and respiratory fitness. These attributes of exercise are key elements to the maintenance of good health and the improvement of athletic performance. But are

Atenolol blunts blood pressure increase during dynamic resistance exercise in hypertensives

This study was conducted to determine whether atenolol was able to decrease BP level and mitigate BP increase during dynamic resistance exercise performed at three different intensities in hypertensives. Ten essential hypertensives (systolic/diastolic BP between 140/90 and 160/105mmHg) were blindly studied after 6 weeks of placebo and atenolol. In each phase, volunteers executed, in a random order, three protocols of knee-extension exercises to fatigue: (i) one set at 100% of 1RM; (ii) three sets at 80% of 1RM; and (iii) three sets at 40% of 1RM. Intra-arterial radial blood pressure was measured throughout the protocols. Atenolol decreased systolic BP maximum values achieved during the three exercise protocols (100% = 186 ± 4 vs. 215 ± 7, 80% = 224 ± 7 vs. 247 ± 9 and 40% = 223 ± 7 vs. 252 ± 16mmHg, P < 0.05). Atenolol also mitigated an increase in systolic BP in the first set of exercises (100% =+38 ± 5 vs.+54 ± 9; 80% =+68 ± 11 vs. +84 ± 13 and 40% =+69 ± 7 vs.+84 ± 14, mmHg, P < 0.05). Atenolol decreased diastolic BP values and mitigated its increase during exercise performed at 100% of 1RM (126 ± 6 vs. 145 ± 6 and +41 ± 6 vs.+52 ± 6, mmHg, P < 0.05), but not at the other exercise intensities. Atenolol was effective in both reducing systolic BP maximum values and mitigating BP increase during resistance exercise performed at different intensities in hypertensive subjects.

Cardiac performance during exercise in hypertensive patients without ventricular hypertrophy

Reduced systolic reserve on effort may be present in subjects with hypertension but no evidence of hypertensive cardiomyopathy. We assessed the determinants of abnormal cardiac performance during exercise in hypertensive patients without left ventricular hypertrophy. Thirty-five newly diagnosed, never-treated-earlier hypertensive patients without definite indication for left ventricular hypertrophy at echocardiography underwent radionuclide ambulatory monitoring of left ventricular function at rest and during upright bicycle exercise testing. The patients were classified into two groups according to their ejection fraction response to exercise. In 21 patients (group 1), the ejection fraction increased > or = 5% with exercise and in 14 patients (group 2), the ejection fraction either increased < 5% or decreased with exercise. Patients of group 1 had lower peak filling rate at rest and less augmentation in end-diastolic volume during exercise (both P < 0.01) when compared with patients of group 2. A significant relationship between the magnitude of change in ejection fraction with exercise and both peak filling rate at rest (r = 0.58, P < 0.01) and exercise-induced change in end-diastolic volume (r = 0.45, P < 0.01) was found. In newly diagnosed, never-treated-earlier hypertensive subjects with no evidence of hypertensive cardiomyopathy, the cardiac response to exercise is dependent on adequate diastolic filling volume to maintain systolic performance.

The cardiovascular effects of upper-limb aerobic exercise in hypertensive patients

Aerobic exercise is broadly recommended as a helpful adjunct to obtain blood pressure control in hypertension. Several hypertensive patients, however, are limited by musculoskeletal complaints or vascular occlusive disease from lower-limb exercise such as jogging or cycling. In the present randomized-controlled study, we evaluate whether an aerobic arm-cycling program provides a measurable cardiovascular benefit. Twenty-four probands were randomly assigned to sedentary activity or a heart rate controlled 12 week exercise program, consisting of arm-cycling at target lactate concentrations of 2.0 +/- 0.5 mmol/l. Endothelial function was assessed by flow-mediated dilation of the brachial artery. Augmentation index and large/small artery compliance (C(1) and C(2)) were measured by computerized pulse-wave analysis of the radial artery. The exercise program led to a significant reduction in systolic (134.0 +/- 20.0 to 127.0 +/- 16.4 mmHg; P = 0.03) and diastolic blood pressure (73.0 +/- 21.6 to 67.1 +/- 8.2 mmHg; P = 0.02) accompanied by a significant improvement in C(2) (3.5 +/- 1.6 to 4.8 +/- 2.0 ml/mmHg x 100; P = 0.004). Flow-mediated dilation, augmentation index, and C(2) were not significantly affected (P > 0.05). Physical performance as derived from lactate and heart rate curves of lower-limb stress tests was unchanged, whereas maximal workload in an upper-limb ergometry significantly increased (P = 0.005). Blood pressure and vascular parameters remained unchanged in the control group. Regular arm aerobic exercise leads to a marked reduction in systolic and diastolic blood pressures and an improvement in small artery compliance. Arm-cycling is a reasonable option for hypertensive patients who want to support blood pressure control by sports despite having coxarthrosis, gonarthrosis, or intermittent claudication.

Phosphodiesterase type 5 inhibition reverses impaired forearm exercise-induced vasodilatation in hypertensive patients

Established hypertension is characterized by increased peripheral vascular resistance and endothelial dysfunction, features that may underlie the reduced exercise-induced vasodilatation seen in hypertensive patients. Sildenafil citrate is a phosphodiesterase type 5 (PDE5) inhibitor used clinically for the treatment of male erectile dysfunction. Its vasodilating properties are due to the inhibition of cyclic guanosine monophosphate (cGMP) breakdown and prolongation of the signalling actions of the nitric oxide (NO)-cGMP pathway in vascular smooth muscle cells. Sildenafil has beneficial effects on endothelial function and exercise tolerance in congestive heart failure and pulmonary hypertension, and we hypothesized that it would improve exercise-induced vasodilatation in hypertensive patients. Ten hypertensive patients and ten matched normotensive subjects were studied in a three-way, randomized, single-blind and placebo-controlled study. On each study day, forearm blood flow (FBF) responses to handgrip exercise were assessed before and after intra-arterial (brachial) infusion of sildenafil, verapamil (a control, cGMP-independent vasodilator), and saline (placebo). Preinfusion exercise-induced vasodilatation was significantly reduced in hypertensive patients compared to normotensive controls. Sildenafil and verapamil infusions both caused a similar increase in baseline FBF. However, while verapamil did not affect the vasodilator response to handgrip exercise in either group, sildenafil substantially enhanced this response in hypertensive patients, but not in normotensive subjects. Our data suggest that sildenafil, through an increase in cGMP levels in the vasculature, substantially and selectively improves the vasodilator response to handgrip exercise in hypertensive patients. These findings represent an essential first step in support of further studies exploring the potentially beneficial effects of PDE5 inhibition on impaired exercise capacity in hypertension.

Coexistence and exercise exacerbation of intraleft ventricular contractile dyssynchrony in hypertensive patients with diastolic heart failure

Patients with heart failure (HF) and a normal left ventricular ejection fraction usually present with diastolic dysfunction (DD). Whether intraleft ventricular contractile dyssynchrony (IVCD) coexists with DD and contributes to the clinical manifestations of HF remains unclear. The study investigated the IVCD at rest and after exercise in hypertensive patients with diastolic HF (DHF). Echocardiography was performed in 60 hypertensive patients with narrow QRS, left ventricular ejection fraction > or = 50%, and no active ischemia. Patients were grouped as having DD (mitral E/A < 1 plus E deceleration time > 200 milliseconds, or mitral annular early diastolic velocity < 8 cm/s; n = 26), DD plus HF symptoms/signs (DHF, n = 13), or as non-DD (n = 21). At rest, the IVCD index (SD of 12 left ventricular segmental electromechanical delays) was greater in the DHF and DD groups than that in the non-DD group (52.2 +/- 10.7 and 39.1 +/- 23.6 vs 23.1 +/- 19.9 milliseconds; P < .05 for both comparisons). Six-minute treadmill exercise induced exacerbation of dyssynchrony in the DHF group (67.0 +/- 12.9 vs 52.2 +/- 10.7 milliseconds; P < .001). Multivariate analysis revealed that the combination of IVCD index > or = 35 milliseconds at rest and > or = 50 milliseconds after exercise was independently associated with DHF (odds ratio = 20, 95% CI = 2-199, P = .009). Postexercise IVCD index correlated positively with plasma N-terminal pro-brain natriuretic peptide (r = 0.37, P = .004). Exercise would aggravate intraventricular dyssynchrony in hypertensive patients with DHF, implicating a potential contribution of systolic dyssynchrony to clinical manifestations.

Attenuation of heart rate recovery after exercise in hypertensive patients with blunting of the nighttime blood pressure fall

Objectives To evaluate whether hypertensive patients with attenuation of nighttime blood pressure (BP) fall exhibit a delay of the recovery of heart rate (HR) after exercise as an index of a general decrease in the vagal tone. Methods Mild-moderate hypertensive patients ( n = 219, age 55 ± 3, 77% men) underwent a maximal exercise test (Bruce > 85% heart rate limited) in whom we calculated the recovery of HR as the percent decrease of HR from peak to 1 min after stopping exercise (%HR fall − 1 min), a 24-h ambulatory BP monitoring, calculating the percent decrease of nighttime vs. daytime BP (% night SBP fall). Left ventricular mass index (LVMI) was measured by echo and aortic stiffness by pulse wave velocity (PWV). Sixty percent were on antihypertensive drugs (not on beta-blockers nor on non-dihydropiridine calcium blockers); 12 subjects were type 2 diabetics. Results: The “% night SBP fall” ranged from − 6.3% to 38.9% and the “%HR fall − 1 min” ranged from 3.3% to 43.7%. There was a significant positive correlation between these two variables ( r = 0.594, p < 0.001). Population was divided into five groups according to quintiles of values for the “% night SBP fall”. For similar daytime BP and age, the lowest quintile for % night SBP fall (− 6.3% to 7.2%) showed the lower “%HR fall − 1 min” (3.1 ± 0.5%), and the higher LVMI (92 ± 3 g/m 2) and PWV (12.1 ± 0.4 m/s) values comparing to the other quintiles ( p<0.02). Conclusions In hypertensives, blunting of the nocturnal fall of BP is associated with a delayed recovery in heart rate after graded maximal exercise and with greater aortic stiffness and ventricular mass. This may indicate that in non-dipper subjects a relative general decrease of parasympathetic reactivation after exercise is linked to the failure of nighttime fall of BP, both of which might contribute to target-organs deterioration.

Response of B-type natriuretic peptide to exercise in hypertensive patients with suspected diastolic heart failure: Correlation with cardiac function, hemodynamics, and workload

Background Diastolic heart failure (DHF) is characterized by dyspnea due to increased left ventricular (LV) filling pressures during stress. We sought the relationship of exercise-induced increases in B-type natriuretic peptide (BNP) to LV filling pressures and parameters of cardiovascular performance in suspected DHF. Methods Twenty-six treated hypertensive patients with suspected DHF (exertional dyspnea, LV ejection fraction >50%, and diastolic dysfunction) underwent maximal exercise echocardiography using the Bruce protocol. BNP, transmitral Doppler, and tissue Doppler for systolic (Sa) and early (Ea) and late (Aa) diastolic mitral annular velocities were obtained at rest and peak stress. LV filling pressures were estimated with E/Ea ratios. Results Resting BNP correlated with resting pulse pressure ( r=0.45, P=0.02). Maximal exercise performance (4.6 ± 2.5min) was limited by dyspnea. Blood pressure increased with exercise (from 143 ± 19/88 ± 8 to 191 ± 22/ 90 ± 10 mm Hg); 13 patients (50%) had a hypertensive response. Peak exercise BNP correlated with peak transmitral E velocity ( r = 0.41, P < .05) and peak heart rate ( r = −0.40, P < .05). BNP increased with exercise (from 48 ± 57 to 74 ± 97 pg/mL, P = .007), and the increment of BNP with exercise was associated with maximal workload and peak exercise Sa, Ea, and Aa ( P < .01 for all). Filling pressures, approximated by lateral E/Ea ratio, increased with exercise (7.7 ± 2.0 to 10.0 ± 4.8, P < .01). BNP was higher in patients with possibly elevated filling pressures at peak exercise (E/Ea >10) compared to those with normal pressures (123 ± 124 vs 45 ± 71 pg/mL, P = .027). Conclusions Augmentation of BNP with exercise in hypertensive patients with suspected DHF is associated with better exercise capacity, LV systolic and diastolic function, and left atrial function. Peak exercise BNP levels may identify exercise-induced elevation of filling pressures in DHF.

Effect of Acute Blood Pressure Reduction on Oxygen Uptake Kinetics at the Onset of Exercise in Hypertensive Patients

The aim of the present study was to investigate the adverse effects of hypertension on the cardiovascular system in daily activities and the effect of acute blood pressure reduction on oxygen (O(2)) uptake kinetics. Twenty hypertensive patients were included in the study group. Patients performed treadmill exercise tests (2.5 km/hour and 5 inclines) twice, before and after blood pressure reduction with sublingual captopril. In the control group, ten hypertensive patients underwent two tests one hour apart without blood pressure reduction brought about by drug therapy. The changes in O(2) kinetic values (O(2) deficit and mean response time [MRT]) between the two tests were investigated. In the study group, the O(2) deficit and MRT values measured during the first exercise testing were found to be 547 +/- 183 mL and 40 +/- 9 seconds, while those in the second exercise testing were 401 +/- 127 mL and 34 +/- 7 seconds, respectively. In the control group, the O(2) deficit and MRT values measured during the first exercise test were 491 +/- 217 mL and 42 +/- 16 seconds and 515 +/- 159 mL and 41 +/- 13 seconds in the second exercise test. The differences in O(2) deficit and MRT in the study group were considered to be statistically significant (P = 0.008 and P = 0.004, respectively). Based on our findings, there was a significant improvement in O(2) kinetic values with an acute reduction in blood pressure in hypertensive patients, most likely as a result of an improved response in cardiac output.

Minimally invasive direct coronary artery bypass (MIDCAB) versus coronary artery stenting for elective revascularization of the left anterior descending artery

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Effect of light exercise on renal hemodynamics in patients with hypertension and chronic renal disease.

Increased physical activity is followed by a stimulation of the sympathetic nervous system and this effect is probably more pronounced in patients with chronic renal failure and hypertension than in healthy controls. The role of sustained exercise in hypertensive patients with chronic renal failure, with and without antihypertensive therapy, is unclear, as is hormonal regulation of the renal hemodynamics. We hypothesized that prolonged low-intensity bicycle exercise would have a greater effect in patients with chronic renal failure than in controls, and that antihypertensive treatment would ameliorate these effects. Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), mean arterial blood pressure (MAP), norepinephrine (NE) and atrial natriuretic peptide (ANP) were measured in the upright position before and during low-intensity exercise for 2 h in healthy controls (n = 8) and in hypertensive patients with moderately reduced renal function who were not taking antihypertensives (n = 7) or who were receiving treatment with captopril (n = 10), enalapril (n = 6) or verapamil (n = 9). GFR tended to decrease and ERPF decreased significantly in healthy individuals when exercise duration was prolonged from 1 to 2 h. An earlier decline in GFR and ERPF was seen in the renal failure patients compared with the controls. Filtration fraction (FF) increased during exercise in all groups except the group taking enalapril. MAP increased in the captopril group during exercise but was unchanged in the other groups. Treatment with captopril produced a more pronounced and earlier fall in exercise-induced GFR than in untreated controls, while verapamil treatment completely blunted the decline in GFR, with a concomitant increase in plasma ANP. No significant changes were seen in plasma NE levels, but urinary NE excretion increased in controls and captopril-treated patients during exercise. The results suggest that prolonged low-intensity exercise has a substantially greater effect on renal hemodynamics in hypertensive renal failure patients than in healthy controls, with negligible changes in plasma NE levels. Verapamil treatment seems to ameliorate the renal effects of exercise on GFR in these patients, and this may in part be mediated via a stimulatory effect on ANP.

Response of blood pressure to maximum exercise in hypertensive patients under different therapeutic programs

To evaluate the behavior of blood pressure during exercise in patients with hypertension controlled by frontline antihypertension drugs. From 979ergometric tests we retrospectively selected 49 hypertensive patients (19 males). The age was 53+/-12 years old and normal range rest arterial pressure (< or = 140/90 mmHg) all on pharmacological monotherapy. There were 12 on beta blockers; 14 on calcium antagonists, 13 on diuretics and 10 on angiotensin converting enzyme inhibitor. Abnormal exercise behavior of blood pressure was diagnosed if anyone of the following criteria was detected: peak systolic pressure above 220 mmHg, raising of systolic pressure > or = 10 mmHg/MET; or increase of diastolic pressure greater than 15 mmHg. Physiologic response of arterial blood pressure occurred in 50% of patients on beta blockers, the best one (p<0.05), in 36% and 31% on calcium antagonists and on diuretics, respectively, and in 20% on angiotensin converting enzyme inhibitor, the later the least one (p<0.05). Beta-blockers were more effective than calcium antagonists, diuretics and angiotensin-converting enzyme inhibitors in controlling blood pressure during exercise, and angiotensin converting enzyme inhibitors the least effective drugs.