Heart failure accompanied by sick euthyroid syndrome and exercise training.

Sick euthyroid syndrome is defined as the decrease of serum free triiodothyronine with normal free L-thyroxin and thyrotropin. Its appearance in patients with chronic heart failure is an indicator of severity. Exercise training through a wide variety of mechanisms reverses sick euthyroid syndrome (normalization of free triiodothyronine levels) and improves the ability to exercise. There is a connection during exercise among dyspnea, hyperventilation, fatigue, catecholamines, a decrease in the number and function of beta-blocker receptors, and elevation of serum free triiodothyronine. It is not known whether sick euthyroid syndrome contributes to the development of heart failure or is only an attendant syndrome.

Risk factors of ischaemic heart disease and long-term outcome after coronary bypass surgery.

BACKGROUND: To investigate the effect of ischaemic heart disease (IHD) risk factors on the long-term course of patients who undergo coronary artery bypass graft (CABG) surgery, was the aim of our study. METHODS: We studied a total of 128 people, who were classified into 4 groups. Control Group A consisted of 24 healthy adults, Group B of 23 patients who underwent CABG for 3-vessel disease and had no complications in the first two postoperative years, Group C of 41 patients who were hospitalized for acute myocardial infarction (AMI) during the first or second post-CABG year and Group D of 40 patients who were hospitalized for AMI without previous CABG. All subjects were investigated for IHD risk factors (blood glucose, serum lipids, lipoprotein-a) with concurrent assays of coagulation-fibrinolysis factors (fibrinogen, antithrombin-III, PAI-1 and t-PA). RESULTS: We found that: 1. Patients with previous CABG represented 50.6% of the total number of patients admitted with AMI in our department during one year. Compared to Groups A (controls) and B (CABG with good course), these patients (Group C) had significant increases in Lp (a), fibrinogen, LDL-ch, PAI-1 and t-PA and decreased HDL-ch and AT-III. 2. There were no significant differences in these factors in patients with AMI, regardless of whether they had had previous CABG. CONCLUSIONS: It is concluded that the accumulation of IHD risk factors and coagulation-fibrinolysis abnormalities play a significant role in the postoperative course of patients undergoing CABG, regardless of the use of anti-angina medication. It is imperative that such factors be corrected.

Comparative haemodynamic responses to the first dose of short- and long-acting ACE inhibitors in patients with congestive heart failure.

BACKGROUND: Angiotensin Converting Enzyme inhibitors (ACEi's) confer significant mortality and morbidity benefits in all functional grades of chronic heart failure (CHF). However, physicians' concerns regarding the possible occurrence of first-dose hypotension appear to be a contributing factor to their under-utilisation in both hospital and primary care settings. We investigated whether long-acting and short-acting ACEi's differ in their haemodynamic responses to the first-dose in patients with CHF. METHOD: This was a multicentre, randomised, open, two-parallel-group study of captopril 6.25 mg and perindopril 2 mg. 240 patients with CHF, age 68.9 +/- 8.9 years, of whom 66% were male, NYHA II-IV, with average blood pressure baseline values of 132.2 +/- 16.2/78.5 +/- 10.5 mmHg for systolic and diastolic blood pressure, and left ventricular ejection fraction (LVEF) of 31.3 +/- 7.4% received either captopril (n = 124) or perindopril (n = 116). Blood pressure was continuously monitored during the 8 h following drug intake. Minimum levels and maximum decreases in systolic, diastolic and mean arterial pressures were measured, along with the incidence of hypotensive episodes defined as mean blood pressure (MBP) fall > 20 mmHg, whether symptomatic or not. Subgroups of patients distributed according to age, baseline blood pressure (BP) and LVEF were subsequently analysed. RESULTS: Overall, a statistically significant treatment effect in favour of perindopril was observed. First-dose hypotension was observed more frequently following captopril than perindopril administration, with lower MAP minimal levels (78.0 +/- 8.9 vs. 84.5 +/- 10.1 mmHg, p < 0.0001), greater maximum falls (17.6 +/- 8.3 vs. 12.8 +/- 7.3 mmHg, p < 0.0001) and more frequent hypotensive episodes (42% vs. 15%, p < 0.0001). The incidence of at least one symptomatic episode was also significantly higher with captopril (10 patients vs. one patient, p = 0.029). Subgroup analyses according to age (< or = 70 years or > 70 years) or LVEF (< or = 30% or > 30%) reflected the main result. CONCLUSION: Initiation of treatment with ACE inhibitors is associated with different haemodynamic and clinical tolerances in CHF patients, regardless of their risk for hypotension, with possible clinical implications.

Alterations in the fibrinolytic system components during acute myocardial infarction.

The purpose of this study was to evaluate the changes in tissue-plasminogen activator (t-PA), plasminogen activator inhibitor - type 1 (PAI-1) and D-dimer (DD) antigen plasma levels in acute myocardial infarction (AMI) patients after thrombolytic therapy with two different thrombolytic agents, rt-PA or acetyl-streptokinase and to find out any correlation between the plasma t-PA, PAI-1 and DD levels with the infarct size as it is estimated from the peak of serum CPK levels. The plasma antigen levels of t-PA, PAI-1 and DD were measured by the enzyme immunoassay method (Stago), in 57 consecutive patients (M = 46, F = 11, mean age 55.6 +/- 8.8 years) and in 25 normal subjects (M = 18, F = 7, mean age 54.0 +/- 5.5 years). In 47 out of the 57 patients who were treated successfully with 100 mg of rt-PA (26 patients) or with 1.5 MU 21 of acetyl-streptokinase, as well as in 10 patients who were not treated, samples were obtained again 4 and 24 hours after the end of thrombolytic therapy or admission, respectively. During the acute phase of myocardial infarction the t-PA, PAI-1 and DD antigen plasma levels were significantly higher than in healthy people. There were no significant changes in the t-PA, PAI-1 and DD plasma levels of the patients who were not treated with a thrombolytic agent. We found a significant elevation of t-PA (p < 0.001), PAI-1 (p < 0.05) and DD (p < 0.001) after 4 hours in comparison with the baseline (at presentation, before therapy). After 24 hours the t-PA and DD plasma levels remained significantly higher (p < 0.001) while the PAI-1 plasma levels returned to the pre-therapy levels. There were no significantly different changes in the t-PA, PAI-1 and DD plasma levels of either group of patients, treated with rt-PA or acetyl-streptokinase while the t-PA and PAI-1 levels were positively correlated with infarct size as estimated from peak serum CPK levels.

Antigenic stimulation in T-cell cultures in cardiomyopathies: differences in cytokine profiles.

Immune-mediated mechanisms are involved in the pathogenesis of cardiomyopathies. In this study, we investigate which pattern of immune response (Th1 or Th2) lies behind these diseases by analysing the basic cytokines secreted from PHA-cultured T lymphocytes and determining what differences, if any, exist between dilated cardiomyopathy (DMC) and hypertrophic cardiomyopathy (HCM). Two groups of patients were studied: 10 patients with DCM and 10 patients with HCM. Age- and sex-matched healthy individuals were used as controls. PHA-cultured T lymphocytes in the presence or absence of different myocardial antigen (MA) concentrations were measured. Interleukine-2 (IL-2), Interleukine-6 (IL-6) and Interferon-gamma (IFN-gamma) levels were measured in culture supernatants by an ELISA method. At the same time, delayed-type hyperactivity (DTH) against the same antigenic preparation was measured by the leukocyte migration inhibitory index technique. Patients were subdivided into DTH-positive and DTH-negative and re-examined for IL-2 cytokine expression. IL-6 levels were found to increase both in the presence and in the absence of MA in the patient groups compared to the controls. IL-2 levels were decreased in both groups, in an antigen dose-related manner. Anergic patients showed a further reduction in IL-2 levels for both groups of patients. IFN-gamma remained unaffected in the patient groups. Almost half of the patients exhibited anergy to the DTH reaction against MA. We conclude that, upon antigenic stimulation, the initially mounted immune response (increased IL-6) is somehow blocked/switched off in patients, resulting in an immunologic tolerance/unresponsiveness to MA (IL-2 decreased, IFN-gamma unchanged). Finally, increased IL-6 could lead to a perpetuation of immunologic injury through the release of oxygen-free radicals with a cytotoxic effect on the myocardium. We hypothesize an antigen-related, defective macrophage-Th1 cell reaction, which accounts for the differences in the IL-2 profile between the DCM and HCM groups, that might cause local immune responses to lead to immunosuppression (immune tolerance effect), thus contributing to the pathogenesis of cardiomyopathies.

Effect of antihypertensive treatment on lipids and fibrinogen: Greek multicentre study of cilazapril.

The effect cilazapril (CLZ) treatment on serum lipids and fibrinogen was studied in 114 hypertensive patients for 18 weeks. Blood pressure, heart rate, lipid profile and fibrinogen were measured before and at the end of the study in all patients. Satisfactory blood pressure control was seen in 68% of the patients (group A) after 4 weeks of treatment with 5 mg CLZ monotherapy, while a single dose of chlorthalidone, 25 mg daily, was added to the therapeutic regimen of the remaining 32% of patients (group B) to achieve blood pressure control. We conclude that CLZ has a slight beneficial effect on the lipid profile and a significantly beneficial effect on fibrinogen, but its combination with a diuretic reverses this beneficial effect.

Immunopathogenic mechanisms in hypertension.

There is a growing interest in immunologically-mediated lesions in the cardiovascular system, as there has been evidence that there are antimitochondrial antibodies (AMA) in patients with hypertrophic cardiomyopathy or hypertensives with left ventricular hypertrophy (LVH). We have also very recently published findings from our laboratory that hypertensives with LVH have a considerable quantity of anticardiac antibodies (ACA) in their serum. The aim of this study was to investigate the possible involvement of autoimmune mechanisms in the pathogenesis and evolution of hypertensive disease. Three groups of subjects were included in the study. Group A comprised 37 patients (20 men, 17 women, mean age 50.5 +/- 8.5 years) with mild to moderate essential hypertension, 19 without echocardiographic evidence of LVH, and 18 with LVH. Group B comprised 10 patients (6 men, 4 women, mean age 45.1 +/- 8.7 years) with secondary hypertension. The control group (C) comprised 15 normotensive subjects (8 men, 7 women, mean age 47.7 +/- 8.7 years). Cellular immunity against arterial wall antigen was studied in all subjects by means of migration inhibitory factor (MIF) against relevant antigen preparation. Sera from Group A and C subjects were tested for the presence of autoantibodies against both specific (myocardial) and nonspecific antigens, by means of the indirect immunofluorescence technique. Eighty per cent of patients with essential hypertension showed a positive cellular response (MIF) against an arterial wall antigen compared to the patients with secondary hypertension or the control group. Moreover, patients with essential hypertension and LVH had the highest incidence of specific (anticardiac, ACA) and nonspecific autoantibodies and the highest C3c and C4 complement component levels compared to patients without LVH or the control group. Most of the ACA positive patients were also AMA positive, while the ACA negative patients were AMA negative as well. Defects in cell-mediated immunity against arterial wall antigen(s) may be the cause or the effect of hypertension. On the basis of our findings that there was no delayed type hypersensitivity response to arterial wall antigen(s) in the patients with secondary hypertension, we suggest that, in some cases of essential hypertension, delayed hypersensitivity reactions possibly contribute to the pathogenesis of hypertension. Autoimmune mechanisms are discussed on the basis of common epitopes shared between heart and arterial tissue.

Intravenous administration of diltiazem in the treatment of supraventricular tachyarrhythmias.

UNLABELLED: The aim of the study was to investigate the efficacy of diltiazem bolus intravenous administration, compared to disopyramide, in the treatment of various types of paroxysmal supraventricular tachyarrhythmias. METHOD: Fifty patients (23 males, 27 females, mean age 47.7 +/- 15.2 years) with paroxysmal supraventricular tachyarrhythmia (20 with paroxysmal atrial tachycardia, 23 with paroxysmal atrial fibrillation and rapid ventricular response and 7 with atrial fluttering) were studied. Diltiazem at a dose of 0.25-0.30 mg/kg BW or disopyramide at a dose of 50 mg were given bolus IV. If conversion of the arrhythmia to sinus rhythm could not be achieved with the initial drug, the alternate was given. The order of administration of the drugs was random, independent of the type of the arrhythmia. Before and during drug administration detailed clinical examination and frequent blood pressure (BP) measurements were performed. Twenty-four hour Holter monitoring was done in all patients, starting with the administration of the antiarrhythmic drug. RESULTS: 1) Paroxysmal atrial tachycardia: diltiazem administration converted the arrhythmia to sinus rhythm in all patients while disopyramide in only 1 of 9 patients who received this drug. 2) Paroxysmal atrial fibrillation: disopyramide converted the arrhythmia in 5 patients without significant change in ventricular response in the others. Diltiazem did not convert the arrhythmia though it caused significant decrease in ventricular response (< 100 bpm) and in 1 patient an important bradycardia (45 bpm). 3) Atrial fluttering: disopyramide converted the arrhythmia to sinus rhythm in 1 patient without significant change in the ventricular response in the others. Diltiazem caused significant decrease in the ventricular response without conversion to sinus rhythm. During conversion to sinus rhythm an AV junctional rhythm of short duration (< 1 min) was noticed in 5 patients and a short pause (< 2 sec) with or without an initial premature contraction in the remaining 21. Disopyramide administration was not associated with side effects. Diltiazem administration cause small (< 20 mm Hg), transient (< 30 min) decrease of BP without symptoms with the exception of the patient with bradycardia in whom the BP decrease was significant (90/60 from 160/80 mm Hg) followed by intense symptoms which lasted for six hours. CONCLUSIONS: Diltiazem administration is extremely effective in conversion of paroxysmal atrial tachycardia to sinus rhythm. In addition it retards ventricular response in patients with atrial fibrillation and fluttering. Compared to disopyramide these effects of diltiazem are more pronounced and clinically pertinent.

The predictive value of troponin T in patients who underwent an extracardiac surgery operation.

UNLABELLED: Purpose of the study is the research of the diagnostic value of the determination of Troponin T in relation with the other cardiac enzymes in patients who underwent extracardiac surgery operation. METHODS: 42 pts (M = 24, F = 18, mean age 51.7 +/- 17 years) who underwent a surgery operation were studies. For all pts serum enzyme CPK, CPK MB, SGOT and Troponin T was determined 24 hours before and after the operation. RESULTS: increased value of CPK was observed in all patients. In 14.3% of pts was found abnormal value of CPK. In 1 pt CPK MB was found increased. In no one of the above pts was observed an increased value of Tr-T. No one of the pts had ECG changes and clinical symptoms indicative of ischemic heart disease. CONCLUSIONS: these results suggest that the determination of Tr-T in serum is more useful diagnostic index for myocardial cell injury in pts who underwent an extracardiac surgery because is not detected in skeletal muscle injury.

The diagnostic value of the determination of troponin T in the diagnosis of unstable angina.

UNLABELLED: The purpose of the study is the predictive value of determination of Tr-T in diagnosis of unstable angina. METHODS: 35 pts (24 male, 11 female, mean age 53.4 +/- 5 years) were studied. Group A: 20 pts (15 male, 5 female, mean age 50 +/- 6 years) with unstable angina. Group B: 15 pts (9 male, 6 female, mean age 56.4 +/- 4 years) with stable angina RESULTS: pts with stable angina (group B) had normal value of CPK-MB, SGOT, LDH, Tr-T. Eight pts with unstable angina (group A) had increased value of Tr-T with normal value of CPK-MB, SGOT, LDH. In conclusion the determination of Tr-T is helpful in diagnosis of unstable angina and it may be useful in the prognosis of these pts.

A possible role for autoantibodies in left ventricular hypertrophy.

The purpose of the study was to investigate the possible role of autoantibodies in the development and type of left-ventricular hypertrophy (LVH). Three groups of subjects were studied: (a) 15 patients with hypertrophic cardiomyopathy (HCM; 11 males, 4 females; mean age 50.0 +/- 16.3 years); (b) 15 patients with essential hypertension (10 males, 5 females; mean age 56.8 +/- 13.5 years) with normal renal function and serum electrolytes and (c) 15 male athletes (mean age 20.8 +/- 5.9 years). The control group consisted of 15 normal subjects with no sign of heart disease. The following indices of cardiac performance were determined by means of echocardiography: end-diastolic and end-systolic diameters, interventricular septum thickness, left-ventricular (LV) wall thickness, LV mass and LV mass index. The immunologic parameters studied included autoantibodies against (a) specific (anticardiac cell; ACA) and (b) nonspecific (antimitochondrial cell; AMA) autoantigens according to a conventional indirect immunofluorescence technique. (1) Higher values for LV mass and LV mass index were observed in HCM. (2) The incidence of specific and non-specific autoantibodies in hypertensive patients and in patients with HCM was significantly higher compared to athletes and controls. All ACA-positive individuals (5 with HCM, 3 with hypertension and 1 athlete) were AMA positive as well, while all ACA-negative individuals were also AMA negative. The ACA-positive individuals had higher C3c and C4 levels compared to the ACA-negative individuals. An autoantibody-mediated immunopathogenic role is discussed in the development and type of myocardial hypertrophy.

Alterations of first derivative of apexcardiogram indices during induced changes of heart rate.

UNLABELLED: The aim of this study is to investigate the effects of HR changes, induced by a variety of causes, on left ventricular performance as assessed by the first derivative of apexcardiogram indices. Ten males, mean age 29.6 +/- 8.1 years, without evidence of heart disease were studied. In all subjects tachycardia was induced by 1) administration of atropine (1 mg bolus IV), 2) administration of isoprenaline (0.5-0.25 micrograms/min IV) and 3) treadmill exercise test according to Bruce protocol. The blood pressure (BP) was determined before and every 60 sec during each test. Drawings of the first derivative of apexcardiogram were obtained before and at the peak of HR and the indices a/b, ef/ZN and b/ef were determined. RESULTS: the increase of HR was similar (about 30% from baseline) in each test. Exercise test caused more pronounced increase of BP compared to the administration of isoprenaline while administration of atropine was not followed by significant changes of BP. Administration of isoprenaline caused similar but more vigorous alterations of the first derivative of apexcardiogram indices (significant increase of b/ef and decrease of a/b and ef/ZN indices) compared with the exercise test. Administration of atropine caused no significant changes of these indices. CONCLUSIONS: in this study it was found that the effects of various causes of tachycardia on LV performance, as assessed by the indices studied, are not uniform; this may reflect different mechanisms involved in the induction of tachycardia by different causes. These results suggest that the alterations of the indices assessed in this study can detect dysfunction(s) of the LV; it is also possible that the type of alteration induced, could provide information regarding causal relationships of this impairment.

Hemodynamic and biochemical changes after chronic administration of cilazapril to hypertensive patients.

The study describes the changes in basic hemodynamic parameters after long-term antihypertensive therapy with cilazapril--a new ACE inhibitor lacking a sulfhydryl group--in hypertensive patients and the drug effects on renal function, glucose tolerance and lipid metabolism. 30 patients (18 males, 12 females, mean age: 53.3 +/- 18 years) with mild to moderate essential hypertension were studied. The following determinations were performed in patients, before and after 4.5 months of cilazapril monotherapy at a dose of 5 mg/24 h: (a) antihypertensive action of the drug (arterial pressure at rest and during a 24-hour recording); drug effects on left ventricular (LV) mass index; its contractility indexes (%FS, EF) and the left atrial emptying index were studied by means of echocardiography; (b) plasma insulin concentration during oral glucose tolerance tests, in the fasting state, after the administration of 75 g glucose per os, as well as the changes in the insulinogenic index and the 6-keto-PGF1 alpha/TXB2 ratio, and (c) drug effect on renal function (urea, creatinine, uric acid, plasma electrolytes), blood lipid profile (total cholesterol, triglycerides, HDL-CH) and serum transaminases. Long-term drug administration exhibits an effective antihypertensive action, without causing reflex tachycardia and also reduces the LV mass index without affecting its EF, while improving its diastolic function. It does not significantly affect the various biochemical parameters, and achieves glucose regulation, both in the fasting state and after glucose loading, with a decrease in the insulinogenic index, and simultaneously increases the 6-keto-PGF1 alpha/TXB2 ratio. The existence of a direct cause-effect relationship between the changes in the above hormone systems is possible.

Influence of left ventricular hypertrophy on the diastolic performance in hypertensive patients and in athletes.

UNLABELLED: The aim of the study was to investigate whether the aetiology of left ventricular hypertrophy (LVH) is related with distinct abnormalities of left ventricular diastolic performance. METHODS: thirty patients with mild to moderate essential hypertension (15 without echocardiographic evidence of LVH and 15 with LVH) and 15 athletes with LVH were studied. Control group comprised 10 normotensive subjects. By means of echocardiography, the dimensions (EDD, ESD) the wall thickness (IVST, PWT) and their ratio (IVST/PWT), the ejection fraction (EF), the mass (LVM) and the index mass (I mass) of the left ventricle (LV) as well as the dimension (LA) and the emptying index (LAEI) of the left atrium were measured. From the first derivative of the apexcardiogram the a/b and ef/ZN indices were estimated. RESULTS: in hypertensive patients, with or without LVH, a decrease of LAEI and increases of a/b and ef/ZN indices were found, compared to normotensive subjects. In contrast, no significant differences were observed between athletes with LVH and normotensive subjects. CONCLUSIONS: in hypertensive patients the diastolic performance of the LV, as derived from the alterations of the indices LAEI, a/b and ef/ZN appears to be impaired at an early stage. This alteration may be related with the increased afterload and diminished diastolic compliance of the LV. In contrast, LV diastolic performance in athletes, even in the presence of LVH, is not affected possibly because fibrosis of the hypertrophic myocardium is less pronounced not affecting LV diastolic compliance.

[The effect of prostaglandins E1 and F1 alpha and indomethacin on haemodynamic and renal endocrine and exocrine function (author's transl)]. / L'effect des prostaglandines E1 et F1 alpha et de l'indométacine sur l'hémodynamique et les fonctions endocrine et exocrine rénales.

1. The PGE1, infused into the renal artery of the dog, increased RPF, Sodium and Potassium excretion rate and UV; it diminished the EPAH and FF but did not alter GFR and PRA. 2. The indomethacin, injected IV, in an other group of animals, decreased RPF, GFR, Sodium and Potassium excretion rate and PRA, and it increased the EPAH and FF. The administration of the PGE1, inversed the results obtained by indomethacin except those of PRA. 3. The infusion of the PGF1a, in other groups of dogs, did not alter either before or after the administration of indomethacin the parameters measured. 4. It was suggested that 1) neither the PGE1 nor the PGF1a stimulated renin synthesis, in the conditions that our experiments took place. The decrease of renin synthesis by indomethacin must be provoked by the inhibition of an other substance than the PGE and PGF and 2) the role of PGE in renal haemodynamic and exocrine renal function seems to be important.

Is low urinary prostaglandin concentration a stage in the development of essential hypertension?

Urinary prostaglandin E and F (PGE and PGF) concentrations, renal plasma flow (RPF), glomerular filtration rate (GFR), sodium excretion rate (UNaV), potassium excretion rate (UKV), urinary osmolarity (Uosm) and osmolar clearance (Cosm) were found to be higher, while mean blood pressure (MBP) was lower in a group of 15 normotensive subjects (15NS), compared to those values obtained in a group of 25 essential patients (25EHP) of the same mean age. After volume expansion, of the 25EHP, urinary PGE concentration, RPF, noncortical plasma flow (NCPF), UNaV, UKV, UNaV/UKV, Cosm and urine volume (UV) increased significantly, MBP, GFR, Uosm, free water reabsorption (Tc water) and urinary aldosterone concentration did not change, while plasma renin activity (PRA) decreased significantly. It was concluded that the deficiency in renomedullary PG synthesis in the EHP is accompanied by a decrease in RPF, NCPF and UNaV. This decrease in UNaV and renal hemodynamics could increase, in the long term, the BP in these patients. Nevertheless, these findings do not exclude the interpretation that the decrease in renomedullary PGE release in the EHP indicates an attempt to increase sodium excretion at the distal tubule by diminishing sodium reabsorption by this agent in order to prevent further increase in BP. In any case, it seems that renomedullary PGs play an important role in intra-renal control systems.

Interaction between aldosterone and renomedullary prostaglandins. Competitive action between aspirin and spironolactone.

Aldosterone injected i.m. decreased the release of renomedullary PGEs and the index (urinary Na/K ratio) in conscious normotensive intact and adrenalectomized rats. Coadministration of spironolactone increased the release of PGEs as well as the index (urinary Na/K ratio). The effect of spironolactone was partly inhibited by aspirin injected in a ratio 5:1 (aspirin:spironolactone), and effect which could be reversed by the infusion of a synthetic prostaglandin (PGA2) in a subhypotensive dose.

Direct relationship between urinary prostaglandin E and sodium excretion in essential hypertensive patients.

Urinary prostaglandins (PGEs and PGFs), sodium and potassium were measured in 17 essentially hypertensive patients. Significant positive correlations were found between a) PGEs secreted in 24 h and sodium excreted in 24 h, b) the ratio PGEs/UnaV before and PGEs/UnaV after volume expansion and c) the ration Na/K and urinary PGEs. It was suggested that renal PGEs, potent natriuretic and diuretic substances, play an important homeostatic role in the extracellular fluid regulation, and consequently in long-term control of the arterial blood pressure.