Left ventricular hypertrophy in rats with renovascular hypertension. Alterations in cardiac function and adrenergic responses.

Performance of the hypertrophied left ventricle was studied by determination of the inotropic response to different stimuli in renal hypertensive rats (two-kidney, one clip Goldblatt, RHR, n = 13) and matched sham-operated controls (NR, n = 11). A model was developed to determine maximal pressure development (transient aortic ligation), maximal pumping ability (rapid transfusion, 2 ml/30 sec), and responses to beta stimulation (isoproterenol, 0.01 to 0.10 micron g/kg/min), using dP/dt/P40 as a load-independent index of contractility. With rapid blood transfusion, RHR developed a higher ventricular systolic pressure (211.5 +/- 10.1 mm Hg vs 194.0 +/- 9.3 (SE), p less than 0.001) but at the expense of higher end-diastolic pressure (LVEDP) (12.2 +/- 1.1 mm Hg vs 7.7 +/- 1.0, p less than 0.02). The maximal response of dP/dt/P40 to isoproterenol was diminished in RHR (29.5 +/- 3.2 sec-1 vs 49.6 +/- 5.2, p less than 0.01) whereas the maximal developed pressure (MDP) was greater in RHR than in NR (239.2 +/- 7.5 mm Hg vs 197.0 +/- 3.9, p les than 0.001). A positive correlation was found between MDP and ventricular weight (r = 0.846, p less than 0.001) in contrast with the negative correlation found between ventricular weight and maximal dP/dt/P40 response to isoproterenol (r = 0.677, p less than 0.001). Thus, cardiac hypertrophy in RHR allowed higher developed ventricular pressures but at the expense of higher LVEDP; at the same time, however, the ability to increase contractility in response to beta adrenergic stimulation was decreased. The contrast in results obtained using different tests of cardiac function indicates the need for a multifactorial approach. It also suggests a subtle transformation in this hypertrophy of the pattern of cardiac adaptation to the increased load.

Impaired cardiac contractile response to isoproterenol in the spontaneously hypertensive rat.

To test the ability of the hypertrophied ventricle to increase its contractility in response to sympathetic stimulation, we compared the chronotropic, inotropic, and relaxation responses to graded in fusions of isoproterenol in spontaneously hypertensive rats (SHR) with responses of matched Wistar-Kyoto (WKY) controls. A closed-chested, direct ventricle puncture was used for the study. The SHR required a higher threshold dose (0.04 vs 0.01 micrograms/kg/min) for a significant chronotropic response, and their maximal response of heart rate was smaller than in WKY (delta HR = +12.5 +/- 5.4 vs +22.8 +/- 10.7 beats/min, p less than 0.01). Contractility indices did not increase in the SHR after isoproterenol infusion: (delta dP/dt +2224.3 +/- 1304.7 mm Hg/sec; delta dP/dt/P = +5.1 +/- 9.3 sec-1, p greater than 0.05) in sharp contrast with the marked increases observed in WKY (delta dP/dt = +4682.1 +/- 435.0 mm Hg/sec, p less than 0.01; delta dP/dt/P +78.6 +/- 8.0 sec-1, p less than 0.001). Left ventricular relaxation rate was marked diminished by isoproterenol in SHR (delta neg dP/dt = -2598.6 +/- 855.0 mm Hg/sec) whereas it was not altered significantly in normotensive rats. Thus, cardiac contractile and chronotropic responses were markedly diminished in SHR, possibly as a result of diminished beta adrenoreceptor mediation; further, the impairment of the relaxation rate induced by isoproterenol in SHR might also interfere with contractile cardiac performance during stress.

Hemodynamic mechanism of blood pressure response to captopril in human malignant hypertension.

The hemodynamic mechanism of blood pressure response to angiotensin blockade is well established in "benign" but not in human malignant hypertension. We studied the changes in mean arterial pressure (MAP), cardiac index (CI), pulmonary wedge pressure (PWP), and in plasma volume (PV) induced by a single oral dose of captopril (150 mg) in 11 patients with malignant hypertension. Two hours after captopril, MAP fell from 178.5 +/- 5.8 to 151.8 +/- 7.8 mm Hg (p less than 0.001) (means +/- SEM) due to a fall in total peripheral resistance (TPR) (from 54.8 +/- 6.8 to 46.4 +/- 1.6 arbitrary units, p less than 0.001). However, there was a simultaneous increase in CI (from 3.29 +/- 0.13 to 3.70 +/- 0.15 liter/min/m2, p less than 0.001), and a decrease in PWP (from 15.3 +/- 3.5 to 11.0 +/- 2.5 mm Hg, p less than 0.001), while PV remained unchanged (from 4.02 +/- 0.26 to 4.12 +/- 0.12 liters, n.s.). Our data show that, in human malignant hypertension, blood pressure response to captopril is due to a decrease in TPR, but in contrast to benign hypertension, there is also a simultaneous increase in CI. Our results suggest that, in malignant hypertension, potentially high CI levels are artificially normalized by the increased TPR and may be fully disclosed by vasodilation.

Anteroventral third ventricle and renin-angiotensin system interaction in the two-kidney, one clip hypertensive rat.

To test the peripheral mechanisms of prevention and reversal of two-kidney, one clip (2K1C) hypertension in the rat by lesion of the anteroventral third ventricle (AV3V) region, we studied blood pressure responses in rats to AV3V lesion produced before (n = 8) or after (n = 8) clipping the left renal artery. Two groups of sham-lesioned, clipped rats (n = 9 each) served as controls. At the end of the experiments, saralasin and captopril were given to evaluate the angiotensin-dependent component of blood pressure. To study the influence of the procedures on plasma renin activity (PRA), two parallel groups of rats (n = 26 and 24, respectively) were submitted to similar surgical protocols. We observed that increases in blood pressure were significantly smaller in the previously lesioned compared to previously sham-lesioned animals (delta BP = 21.5 +/- 3.7 vs. 32.9 +/- 2.5 mm Hg, p less than 0.01); also, AV3V lesion almost completely reversed hypertension (BP from 167.5 +/- 2.9 to 136.0 +/- 4.1 mm Hg, p less than 0.001), which was not observed in the sham-lesioned animals (BP from 172.0 +/- 2.8 to 168 +/- 2.7 mm Hg, NS). Saralasin produced a significantly smaller decrease in BP in the lesioned animals compared to those with sham lesions during both prevention and reversal experiments. Similar results were observed with captopril. Previous AV3V lesion did not significantly affect PRA with clipping of the renal artery, but AV3V destruction after hypertension had been established resulted in significantly lower PRA compared to sham-lesioned animals (4.58 +/- 0.72 vs 8.38 +/- 1.79, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Methylprednisolone-induced hypertension. Role for the autonomic and renin angiotensin systems.

The role of the autonomic nervous system (ANS) in the pathogenesis of hypertension induced by methylprednisolone (20 mg/kg/week subcutaneously) was studied in rats before and during chronic renin angiotensin system (RAS) blockade with captopril (20 mg/kg/every 8 hrs by mouth). Sympathetic nervous system (SNS) blockade was accomplished by the intravenous (i.v.) administration of propranolol (0.20 mg/100g) plus phentolamine (1.25 mg/100g/i.v.) and ganglionic (G) blockade by the use of pentolinium tartarate (0.5 mg/100g/i.v.). After 4 weeks, methylprednisolone-treated animals showed significant decreases in mean arterial pressure (MAP) with both SNS (-34 +/- 2 mm Hg) and G (-56 +/- 3 mm Hg) blockades; during chronic RAS blockade, even greater falls in MAP were observed (SNS = -43 +/- 2 mm Hg and G = -75 +/- 3 mm Hg). Nevertheless, for both groups the levels of MAP obtained during SNS and G blockades were higher than those observed in their control groups. At the end of second week, however, in captopril-treated hypertensive rats the values of MAP obtained during ANS blockade were lower than those observed in the control group. An increased responsiveness to exogenous administration of norepinephrine (NE) was observed in animals receiving methylprednisolone and captopril. It is concluded that methylprednisolone hypertension in the rat may be initially explained by activation of RAS and ANS. At later phases, a third mechanism has to be postulated to explain the hypertensive state.

Effects of a specific inhibitor of the vascular action of vasopressin in humans.

Experimental evidence indicates that arginine vasopressin (AVP) may contribute to the rise of blood pressure (BP) in hypertension induced by renal failure and sodium overload. We studied the AVP inhibitor [1-(B-mercapto-B,B-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine] AVP in 12 normal and seven hypertensive subjects with end-stage renal disease. To test the agent's capacity to block the pressor action of exogenous AVP In humans, we constructed a dose-response curve with AVP doses of 1 to 20 mU/kg, raising BP by up to 30 mm Hg. Subsequently, five volunteers receive intravenous (i.v.) doses of 0.1 mg, and five volunteers received 0.5 mg of the inhibitor. The dose-response curve was then repeated with AVP doses up to 200 mU/kg. Both doses of the inhibitor shifted the curve to the right and downward, with the BP response to 20 mU/kg AVP being inhibited by 23% and 80% respectively. The duration of action of the compound was tested in two additional subjects, and was found to be over 3 hours. We then tested the compound in seven hypertensive patients with end-stage renal failure. Two days before dialysis, patients received a 150 mEq/day Na diet. After an additional Na load of 180 mEq via i.v. saline over 3 hours under constant BP and ECG monitoring, they received an i.v. bolus of 0.5 mg AVP inhibitor. A moderate BP fall occurred in five patients; it was maximal at 45 to 60 minutes and returned to baseline by 70 to 90 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

A reevaluation of the hemodynamics of pheochromocytoma.

We examined the hemodynamic features of 24 untreated patients with surgically proven pheochromocytoma during steady-state periods and compared them with 24 untreated essential hypertensive patients individually matched for sex, age, body surface area, and arterial blood pressure. We found that, despite having 10-fold higher levels of circulating catecholamines, pheochromocytoma patients have hemodynamic characteristics similar to patients with essential hypertension and that, in individual patients, the ratio of circulating norepinephrine to epinephrine had no relation to the hemodynamic profile. In both groups, increased total peripheral resistance is primarily responsible for maintenance of hypertension. These results suggest that, unlike the acute administration of catecholamines, long-term exposure to high levels of circulating catecholamines does not produce hemodynamic responses characteristic of this group of compounds. This might be due in part to desensitization of the cardiovascular system to catecholamines and might explain the clinical observation that some patients can be completely asymptomatic despite harboring an actively catecholamine-secreting pheochromocytoma.

Pindolol, not propranolol, reverses cardiac hypertrophy in renal hypertensive rats.

Reversal of cardiac hypertrophy has been obtained by treatment with some antihypertensive drugs but has not been achieved consistently with beta blockers. To investigate whether this difference might be explained by the distinct hemodynamic actions of the drugs, we studied the effects of propranolol and pindolol, beta blockers with distinct modes of action, on cardiac hypertrophy of hypertensive male Wistar rats, two-kidney, one clip (2K1C) Goldblatt model (n = 33) and sham-operated control rats (n = 34). We also assessed the effects of such therapies on the ventricular pumping ability during open-chest, transient aortic occlusion. Four weeks after surgery, propranolol (5 mg/kg/day p.o.) was given to hypertensive (n = 8) and control rats (n = 11); pindolol was also given orally (1 mg/kg/day) to similar groups (n = 7 and n = 5, respectively). Untreated animals served as controls for both groups. Cardiac hypertrophy developed with hypertension in the untreated rats of the propranolol (3.38 +/- 0.18 vs 2.60 +/- 0.08 mg/g; p less than 0.01) and pindolol groups (3.93 +/- 0.21 vs 2.40 +/- 0.03 mg/g; p less than 0.001). Treatment reversed cardiac hypertrophy in the pindolol-treated (3.01 +/- 0.19 vs 3.93 +/- 0.21 mg/g; p less than 0.001, NS) but not in the propranolol-treated rats (3.24 +/- 0.18 vs 3.38 +/- 0.21 mg/g, NS). The maximal pressure that developed during aortic occlusion in the propranolol group was similar to that observed in the pindolol group. These results indicate that cardiac hypertrophy is reversed by pindolol but not by propranolol, and that this reversal does not interfere with left ventricular pumping ability.

Severe hypertension induces disturbances of renal autoregulation.

To study if the severity of hypertension could be associated with disturbances of the autoregulation of renal blood flow and glomerular filtration, we compared the renal hemodynamic and functional responses to acute blood pressure reductions of a group of patients with moderate essential hypertension (n = 10) with those of a group of patients with severe hypertension (n = 10). Blood pressure was reduced to normal levels by a stepwise infusion of sodium nitroprusside, and effective renal blood flow (by 131I-hippuran), glomerular filtration rate (by endogenous creatinine clearance), and filtration fraction were determined. After acute blood pressure normalization, effective renal blood flow and glomerular filtration rate were significantly reduced in patients with severe hypertension (-41.6 +/- 8.3% and -44.7 +/- 6.8%, respectively; p less than 0.01 for both) but not in those with moderate hypertension (+4.9 +/- 9.1% and +6.2 +/- 13.3%, respectively; NS). Filtration fraction remained unchanged in both groups. These results show that severe but not moderate essential hypertensive patients have a displacement to the right of the lower limit of the renal autoregulation curve due to impaired vasodilation to maintain adequate renal blood flow during acute reductions of blood pressure. This impairment may be due to anatomic or functional defects of preglomerular vessels, or to both. Furthermore, the inability to maintain adequate glomerular filtration in these circumstances shows that patients with severe hypertension also have an impaired ability to adjust postglomerular vasomotor tone in the face of reductions in glomerular blood flow.

Malignant hypertension: a syndrome accompanied by plasmatic diminution of low and high molecular weight kininogens.

Total kininogen (Kgn), kallikrein, and prekallikrein were measured in patients with malignant hypertension (MH), essential hypertension (EH), normotensive control (NC), and hypertension and chronic renal failure (HRF). These components of the kallikrein-kinin system were related to the levels of creatinine and fibrinogen. High molecular weight Kgn and low molecular weight Kgn were also measured in blood samples from a peripheral vein, arterial blood, and suprahepatic vein in NC, EH, and MH. Results showed that total Kgn levels were diminished in MH and this diminution could not be ascribed to decreases in renal function, hematocrit, or fibrinogen levels. Appropriate antihypertensive treatment for over 1 year did not normalize Kgn levels in 10 of 11 patients. High molecular weight Kgn and low molecular weight Kgn were both diminished in MH (0.26 +/- 0.04 nmol bradykinin/ml and 0.93 +/- 0.12 nmol lysyl-bradykinin/ml, respectively) as compared to NC (0.39 +/- 0.07 and 1.92 +/- 0.16) and EH (0.51 +/- 0.07 and 1.65 +/- 0.13). Higher concentrations of high molecular weight Kgn were demonstrated in the suprahepatic vein as compared to arterial blood, demonstrating its synthesis by the liver. However, patients with MH had a diminished capacity to synthetize high molecular weight Kgn. A decrease in synthesis of high molecular weight Kgn may be a partial explanation for low levels of total Kgn. It is suggested that a lack of Kgn may play a role in the pathogenesis of MH.

Hypertension and economic activities in São Paulo, Brazil.

A study of the prevalence of hypertension was undertaken among workers in 10 subsectors of the economy in São Paulo, a major urban-industrial area of Brazil. Included in the study were 5500 subjects 15-65 years of age, employed in 57 randomly selected firms. Hypertension rates (DBP greater than or equal to 90 mm Hg) were higher among males up to 44 years of age. There was a decreasing gradient from mild to moderate and severe forms in all groups. Severity tended to increase with age in all groups. Black males showed higher rates than whites (29.2% vs 16.7%, p less than 0.05), the excess being partially accounted for by moderate and severe forms (40% vs 20%). Subjects who overworked showed a trend toward higher hypertension rates. Higher rates in four subsectors (metallurgy, finance, transport, and journalism), aside from the distribution of known risk factors and job selection, may reflect a variety of work-related stressors.

Acute hemodynamic and humoral effects of metoclopramide on blood pressure control improvement in subjects with diabetic orthostatic hypotension.

Metoclopramide (MCP), a dopaminergic antagonist, is effective in postural hypotension, but the mechanisms of action have not been well defined. We studied responses of mean arterial pressure (MAP), heart rate, cardiac output (CO), and total peripheral resistance (TPR) after 5 min of increasing degrees of head tilt (15 degrees to 90 degrees) before and after MCP (20 mg IV) in seven subjects with diabetic postural hypotension. Plasma renin activity (PRA) and plasma aldosterone levels (PA) were determined at each degree of tilt; responses to the cold pressor test were also assessed before and after MCP. Before MCP, the maximal degree of tilt tolerated was 75 degrees, while after MCP four subjects were able to support 90 degrees tilt. At 45 degrees tilt, the decreases in MAP were smaller after than before MCP (-7.6 +/- 3.3 and -28.1 +/- 8.5 mm Hg; means +/- SE). This was associated with responses of TPR to tilt after (from 18.6 +/- 2.6 to 24.0 +/- 3.9 arbitrary units [AU]) but not before (from 22.9 +/- 4.0 to 25.6 +/- 4.5 AU) MCP. Reductions in CO were of the same order before and after MCP. PRA responded to tilt better after than before MCP. Supine PA levels increased with MCP (delta PA = 5.4 +/- 0.7 ng/dl), but its response to tilt was unaltered. There were significant rises in MAP and HR during the cold pressor test after but not before MCP. Our data suggest that vasoconstriction is the main mechanism of MCP improvement in blood pressure response to an orthostatic stimulus in diabetic postural hypotension, possibly because of its antidopaminergic property.

The renin-angiotensin system in the control of systemic arterial pressure.

The renin-angiotensin system through its active octapeptide, angiotensin II, has an important role in systemic arterial pressure control. Angiotensin II is a potent direct vasoconstrictor and is also the main regulator of aldosterone secretion. The complete analysis of the role of angiotensin II has to take into account the prevailing sodium balance for a given level of angiotensin II and also its indirect action upon the sympathetic nervous system as well as other hormonal systems. A number of studies have provided evidence for an important role for the renin-angiotensin system in renovascular hypertension, malignant and severe hypertension, as well as in mild to moderate forms of essential hypertension.

Reversal of left ventricular hypertrophy with isradipine induces diminution of cardiac arrhythmias.

The left ventricular hypertrophy (LVH) of hypertension is often associated with ventricular arrhythmias, which may increase the risk of cardiovascular mortality. Our study was therefore designed to assess whether pharmacological reversal of LVH was associated with the diminution of LV ectopic beats. The antihypertensive agent selected for the study was the dihydropyridine calcium antagonist isradipine (2.5 to 5.0 mg/day orally), which induces rapid regression of LVH. A marked temporal association was observed between regression of LV mass and reductions in the total number of ventricular extrasystoles and in paired beats. Furthermore, there was a diminution of the complexity of the form of ventricular ectopic beats during antihypertensive treatment. No changes in serum electrolytes were documented to account for this control of cardiac arrhythmias. We conclude that the reversal of LVH obtained with isradipine is accompanied by control of the ventricular arrhythmias in hypertensive patients. It is possible that this cardioprotective action may be associated non-specifically with the reduction in LV mass, although a drug- or class-specific action cannot be ruled out.

Regression of left ventricular hypertrophy in the short-term treatment of hypertension with isradipine.

This was a study of the effectiveness of isradipine, a calcium antagonist of the dihydropyridine group, in reversing left ventricular hypertrophy (LVH) in patients with mild-to-moderate hypertension. Mean arterial pressure was effectively reduced at 90 days of treatment (from 129.5 +/- 2.0 to 111.5 +/- 2.8 mm Hg; P less than .001). The electrocardiographic Romhilt-Estes score for LVH showed early reduction at 45 days of treatment (from 7.1 +/- 0.6 to 5.1 +/- 0.4 points; P less than .001), and further diminutions were observed at 90 days of treatment (3.8 +/- 0.4 points; P less than .01). The echocardiographically determined left ventricular mass indices confirmed these findings (from 175.0 +/- 8.9 to 141.7 +/- 5.5 and to 124.8 +/- 4.2 g/m2; P less than .001) for 45 and 90 days, respectively. The results indicate that isradipine is effective in reducing left ventricular mass and that these reductions are observed early in the course of treatment.

Parenteral isradipine reduces blood pressure in hypertensive crisis.

The efficacy and tolerability of an infusion of isradipine, a calcium antagonist of the dihydropyridine type, were tested in patients in hypertensive crisis. Ten patients with symptomatic and significant elevations in blood pressure were infused for 12 h with isradipine at 1.2, 2.4, 4.8, and 7.2 micrograms/kg/h (3 h of each infusion level). No untoward effects or adverse reactions were noted. No alterations were observed on electrocardiographic tracings, and blood pressure was significantly reduced only at doses of 7.2 micrograms/kg/h. Thus, isradipine as an infusion is useful and safe for hypertensive crisis, starting at a rate of 7.2 micrograms/kg/h. Higher doses may yet prove to be safe, well tolerated, and even more efficacious.

Comparison of the hemodynamic effects of sodium acetate in euvolemic dogs and in dogs submitted to hemorrhagic shock.

We determined the dose-response relationship of systemic hemodynamics with graded intravenous infusions of sodium acetate (0.75, 1.50 and 3.00 microEq kg-1 min-1) in a group of dogs in the euvolemic state (N = 10) and in animals submitted to severe hemorrhagic shock (N = 7). Sodium acetate had a marked vasodilator effect on both groups, decreasing total peripheral resistance by 36.6% and 55.1%, respectively. Cardiac index increased simultaneously by 68.4% and 143.0%, respectively. Sodium acetate induced an approximate normalization of cardiac index and peripheral resistance at the highest infusion rate in the animals submitted to hemorrhagic shock. The normalization of cardiac output was due to a marked increase in heart rate in euvolemic dogs and to an increase in stroke volume in shocked animals. The hyperkinetic state of the circulation induced by the drug and a possible inotropic action of sodium acetate either direct or indirect could explain the different patterns of response.

Risk factors for the occurrence of cardiac arrhythmias in patients on continuous ambulatory peritoneal dialysis.

In order to evaluate the risk factors for the occurrence of ventricular arrhythmias (VA) in continuous ambulatory peritoneal dialysis (CAPD), we studied 47 patients by echocardiography, dipyridamole-thallium tests, and biochemical profile. We observed that the group with VA had a greater cardiac mass index dependent only on an increased left ventricular internal diameter. Septum and posterior wall thickness, as well as biochemical variables, were not associated with the presence of VA in CAPD patients. In addition, altered myocardial perfusion was not associated with VA in these patients.

[Reversal of left ventricular hypertrophy after the use of benazepril]. / Reversão de hipertrofia ventricular esquerda após o uso de benazepril.

PURPOSE: To assess the effects of benazepril (ACE inhibitor) on arterial blood pressure (ABP) and left ventricular mass index (LVMI). METHODS: Nineteen patients (7 men, 12 women) with mean age 38.2 +/- 10.2 years, with mild to moderate hypertension were evaluated. Besides raised blood pressure, the necessary inclusion criterion was the presence of left ventricular hypertrophy detected by echocardiogram. After a wash-out period, all patients were given placebo followed by the active drug benazepril at a dose of 10 mg once a day. For those patients who did not achieve a satisfactory control of the blood pressure (BP) 25 mg of chlorthalidone was added. All patients underwent 180 days of benazepril treatment. RESULTS: The ABP was gradually controlled as follow: at seated position the systolic BP changed from 156.05 +/- 5.07 mmHg to 129 +/- 3.74 mmHg (p < 0.001) and the diastolic BP from 99.74 +/- 1.59 mmHg to 81.8 +/- 2.27 mmHg (p < 0.001). At orthostatic position the systolic BP changed from 156.9 +/- 5.35 mmHg to 124.28 +/- 5.33 mmHg (p < 0.001) and the diastolic BP from 101.7 +/- 1.34 to 81.36 +/- 2.81 (p < 0.001). The heart rate did not change significantly during the study. The LVMI decreased significantly from 182.4 +/- 9.2g/m2 to 122.6 +/- 4.2g/m2 (p < 0.001). CONCLUSION: Our data revealed that 100% of the patients achieved satisfactory degrees of LVMI regression and in 34% there was a normalization of it.

[Captopril in the treatment of patients with congestive heart failure. Its bicycle ergometry evaluation]. / Captopril no tratamento de pacientes com insuficiência cardíaca congestiva. Avaliação cicloergométrica.

PURPOSE: To analyze the physical performance of the patients with congestive heart failure (CHF), grades I and II of the New York Heart Association (NYHA), submitted to ergometric test: 1) under conventional treatment with digitalis and diuretic; 2) with an angiotensin converting enzyme inhibitor, captopril, associate with conventional treatment; 3) using captopril associated with digitalis or diuretic. METHODS: A randomized double blind study was performed in 20 patients with CHF (I and II-NYHA) submitted to ergometric test in different therapeutic phases. The initial workload was 5 watts and load was increased until the appearance of limiting symptoms. RESULTS: The introduction of captopril to the conventional treatment for CHF or associated with digitalis or diuretic promotes significant increase in the duration of the physical exercise, in the oxygen consumption and in the total workload during the ergometric test. CONCLUSION: In the initial forms of CHF, captopril provides better physical performance when compared with conventional treatment and the diuretic treatment can be changed for the angiotensin converting enzyme inhibitor with equal efficacy.