Effect of isobaric hyperoxemia on erythropoietin secretion in hypertensive patients.

We assessed the influence of hyperoxemia on erythropoietin secretion in patients with various etiological forms of arterial hypertension (essential, n = 15; renoparenchymal, n = 16; renovascular, n = 15) and in 15 healthy subjects. On the first day of the study, blood was withdrawn at 1-hour intervals for the estimation of erythropoietin during a total of 6 hours and at 2-hour intervals for the assessment of PO2. Three days later the same parameters were assessed again at identical time intervals, but the subjects were breathing pure oxygen during the first 2 hours. Breathing with pure oxygen resulted in a significant increase of blood PO2 (184.85 +/- 4.47 versus 85.92 +/- 2.28 in essential, 185.21 +/- 5.52 versus 84.55 +/- 3.04 in renoparenchymal, and 181.7 +/- 3.14 versus 87.49 +/- 2.25 in renovascular hypertension groups and 189.84 +/- 5.2 versus 85.89 +/- 1.73 mm Hg in healthy subjects; P < .001 in all groups). Baseline plasma erythropoietin was not different among the groups (29.33 +/- 4.14 in essential, 24.56 +/- 3.09 in renoparenchymal, and 27.77 +/- 3.29 in renovascular hypertension groups and 24.23 +/- 2.70 mU/mL in the control group). The pattern of erythropoietin decline was different in the groups of hypertensive patients. In patients with essential hypertension, unlike in healthy subjects and patients with other etiological forms of arterial hypertension, only a very short-term suppression of erythropoietin levels was observed during hyperoxemia. No significant changes in blood pressure during breathing with pure oxygen were found in any of the studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of IFN-alpha on plasma erythropoietin levels in patients with hepatitis B virus-associated chronic active hepatitis.

The influence of 3-month interferon-alpha (IFN-alpha) treatment on plasma erythropoietin (EPO) concentration in patients with chronic active hepatitis (CAH) induced by hepatitis B virus (HBV) infection was investigated. The study was carried out in 44 nonanemic patients divided into two groups: CAH B, 30 subjects not treated with IFN-alpha, and CAH B-IFN, 14 subjects treated with IFN-alpha for the first 3 months of the study (5 MU/m(2) body surface subcutaneously (s.c.) three times per week). In all patients, blood samples were taken at the beginning of the study (0) and after 1, 2, 3, 6, 9, and 12 months of observation. At the beginning, plasma EPO levels in the CAH B (27.8 +/- 2.21 mU/ml) and CAH B-IFN (27.3 +/- 3.04 mU/ml) groups did not differ significantly from each other and were significantly higher (p < 0.0001) than in healthy subjects (10.4 +/- 1.06 mU/ml). In patients in the CAH B group, plasma EPO concentrations did not change significantly during the whole observation period. In patients in the CAH B-IFN group, a transient, significant increase in plasma EPO level was found. The highest plasma EPO concentration in this group was noted after the third month of treatment (41.1 +/- 3.41 mU/ml). In conclusion, patients with CAH induced by HBV infection are characterized by increased plasma EPO concentrations, and IFN-alpha treatment in these patients causes a transient increase in the plasma EPO level.

Effect of early captopril treatment on blood adrenaline levels in acute myocardial infarction (the substudy of ISIS-4). International Study of Infarct Survival-4.

Of patients with acute myocardial infarction eligible for the International Study of Infarct Survival-4, randomized to captopril (n = 30) or placebo (n = 33), the captopril group had a significant decrease in blood adrenaline on day 3 compared with baseline values. Results suggest that suppression of sympathetic activity contributes to the beneficial effects of treatment with angiotensin-converting enzyme inhibitors in the early phase of acute myocardial infarction.

Effects of acute euglycemic hyperinsulinemia on urinary nitrite/nitrate excretion and plasma endothelin-1 levels in men with essential hypertension and normotensive controls.

Insulin stimulates the production of endothelin-1 (ET-1) and nitric oxide (NO) by isolated endothelial cells. Additionally, insulin-dependent glucose transport and insulin-mediated NO production partially share common elements in signal transduction. There are discordant data on plasma ET-1 levels during acute euglycemic systemic hyperinsulinemia in normotensive men and men with essential hypertension (EH) (known to be insulin-resistant), as well as on the relations between insulin sensitivity and vascular function. Our aim was to assess the response of approximate measures of whole-body generation of NO and ET-1 to acute euglycemic hyperinsulinemia in EH patients and controls. We studied 17 newly diagnosed untreated men with uncomplicated EH and 10 normotensive controls. Plasma ET-1 and urinary excretion of nitrite plus nitrate, stable NO metabolites (Uno(x)), were measured before and during a 3-hour hyperinsulinemic-euglycemic clamp. Both in hypertensives and normotensives, plasma ET-1 levels were reduced after 2 hours of the clamp (EH: baseline, 3.1+/-1.9 pg/mL; 2 hours, 1.9+/-1.2 pg/mL, P = .04 v baseline; controls: baseline, 4.2+/-2.6 pg/mL; 2 hours, 2.8+/-1.4 pg/mL, P = .04 v baseline). No significant changes in Uno(x) during the clamp were observed. Changes in Uno(x) during the clamp (deltaUno(x)) and differences in plasma ET-1 measured before the end and before the beginning of the clamp (deltaET-1) were correlated in the controls (r = .75, P = .01) but not in EH (r = -.01, P = .97). No parameter of glucose metabolism correlated with basal Uno(x), basal plasma ET-1, deltaUno(x), and deltaET-1, whether absolute or percent values, in either group. Thus, acute euglycemic hyperinsulinemia produces a decrease in plasma ET-1 in both EH patients and controls. The lack of correlation between deltaUno(x) and deltaET-1 under these conditions in EH may suggest an impairment of systems governing interactions between the NO-dependent pathway and ET-1. In addition, insulin actions on glucose metabolism and on the endothelial mediators appear dissociated.

Influence of ultraviolet irradiation on plasma vitamin D and calcitonin levels in humans.

In 13 patients with essential hypertension (EH) and in 10 normotensive controls, the influence of ultraviolet irradiation on plasma calcium, phosphorus, 25-OH-D, 1,25(OH)2D and calcitonin (CT) was studied. The basal levels of total calcium (2.47 +/- 0.02 mmol/liter) and phosphorus (1.10 +/- 0.04 mmol/liter) in patients with essential hypertension were not different from the control subjects (2.49 +/- 0.05 mmol/liter and 1.22 +/- 0.06 mmol/liter, respectively). However, patients with essential hypertension had elevated levels of 25-OH-D (68.09 +/- 7.48 vs. 26.51 +/- 3.3 mg/ml), 1,25(OH)2D (175.15 +/- 32.5 pmol/liter vs. 118.0 +/- 13.23 pmol/liter) and CT (131.7 +/- 32.36 pg/ml vs. 49.0 +/- 18.62 pg/ml) than in control subjects. In contrast to normotensive subjects, the majority of hypertensive patients showed no rise of plasma 25-OH-D and 1,25(OH)2D in response to ultraviolet irradiation. The results of this study suggest involvement of abnormal vitamin D metabolism in the pathogenesis of hypertension, at least in some patients.

Pharmacokinetics of ritanserin in patients undergoing hemodialysis.

The pharmacokinetics of ritanserin were studied in five patients with chronic renal insufficiency and who were undergoing periodic hemodialysis. Immediately after breakfast, a single 10-mg ritanserin tablet was administered to each patient on a day that they did not undergo dialysis. Plasma ritanserin levels were measured by a specific high-performance liquid chromatographic assay sensitive to 2 ng/mL plasma. After the oral 10-mg dose, the average time to reach the peak plasma concentration, Tmax, was 4.4 +/- 2.2 hours in these uremic patients, with a range of 2 to 8 hours. The average peak plasma concentration was 73.6 +/- 26.9 ng/mL (range: 54.6-120.0 ng/mL). Compared with a previous study in healthy volunteers, the uremic patients had a slower absorption profile, with a 39% reduction in peak plasma concentration and mean delay of 2.5 hours in Tmax. The mean area under the plasma concentration-time curve for ritanserin (2031 +/- 636 ng.hr/mL) was 47% lower compared with that in healthy volunteers (3867 +/- 1413 ng.hr/mL). The observed delayed and lower ritanserin absorption in these uremic patients may be caused by the chronic use of antacids such as aluminum hydroxide and calcium carbonate in all patients and/or by concurrent pathologic changes in the gastrointestinal mucosa of these patients. The regular hemodialysis sessions every 2-3 days did not affect the elimination rate of ritanserin, as the terminal half-life in these patients (39 +/- 23 hr) is similar to that in healthy volunteers (41 +/- 14 hr).

Urinary excretion of Tamm-Horsfall protein in normotensive and hypertensive elderly patients.

Tamm-Horsfall protein (THP) is a glycoprotein that is exclusively produced by the kidney in the thick ascending limb of Henle's loop (TAHL). Disturbances of TAHL function are associated with decreased urinary THP excretion. It is well known that renal function declines with advancing age. Moreover, it is suggested that THP may play a role in the pathophysiology of hypertension. The aim of this study was to assess urinary excretion of THP (U-THP) in healthy and hypertensive elderly patients. Fifteen young healthy subjects (YHS), 15 young hypertensive patients (YHT), 15 older normotensive (>60 years) subjects (OHS) and 31 older (>60 years) hypertensive patients (OHT) were examined. In all subjects 24-h urinary volume (UV), U-THP and creatinine (U-Cr), specific gravity of urine (U-SG), serum creatinine (S-Cr), and mean arterial pressure (MAP) were assessed. THP urinary excretion was significantly decreased in normotensive elderly patients, but not in hypertensive ones. Higher U-THP in the elderly hypertensive as compared with the elderly normotensive patients seems to be more the consequence than the cause of arterial hypertension.

Relationship between plasma renin profile and leptinaemia in patients with essential hypertension.

Both leptin and the renin-angiotensin system (RAS) can influence the activity of the sympathetic nervous system, water and electrolyte metabolism as well as vascular remodelling, which are all involved in the regulation of arterial blood pressure. Thus leptin and the RAS may act together in the pathogenesis of essential hypertension. The present study aimed to answer the following question: does an interrelationship exist between leptinaemia and the plasma renin activity (PRA) profile in normotensive and hypertensive subjects? Forty-three patients with essential hypertension (EHP) (23 females, 20 males, mean age 39.0 +/- 1.8 years, mean body mass index (BMI) 26. 8 +/- 0.6 kg/m2, mean arterial pressure (MAP) 123 +/- 2 mm Hg) and 32 healthy subjects (NTS) (18 females, 14 males, mean age 38.6 +/- 2. 2 years, mean BMI 25.4 +/- 0.5 kg/m2, MAP 95 +/- 1 mm Hg) were examined. Plasma leptin levels were estimated once after the administration of a diet containing 100-120 mmol Na/day and after overnight 8-h recumbency. PRA was estimated twice: first after the administration of a diet containing 100-120 mmol Na day and overnight 8-h recumbency (PRA I), and a second time after 3 days of sodium restriction (20 mmol Na/day), and 3 h of upright position (PRA II). Antihypertensive drugs were withdrawn 7 days before the study. In EHP plasma leptin concentration was insignificantly higher than in NTS (14.0 +/- 2.0 vs10.8 +/- 1.5 ng/ml respectively). Only females with hypertension showed a significant positive correlation between plasma leptin concentrations (expressed as the logarithmic values) and PRA I. Using the multiple regression analysis, in all studied subjects (EHP and NTS together), logarithm (log) of plasma leptin concentrations was significantly related to gender, BMI and MAP. Multiple regression analysis performed separately for EHP or NTS revealed a significant relation of log plasma leptin concentrations with gender and BMI. A significant correlation was found between log leptinaemia values and BMI, mean and systolic blood pressure respectively if the whole group of subjects (EHP+NTS) or EHP and NTS separately were analysed. Especially in hypertensive women a highly significant correlation was found between log plasma leptin concentrations and MAP. We conclude that a significant relationship between leptinaemia and PRA does exist in females with EH and that participation of both PRA and leptin in the pathogenesis of EH in females seems to be likely.

Interrelationship between plasma leptin concentration and severity of metabolic acidosis in haemodialysed patients with chronical renal failure.

Patients with chronic renal failure are frequently characterized by malnutrition, hyperleptinaemia and metabolic acidosis. Both hyperleptinaemia and chronic metabolic acidosis are presumed to contribute to the pathogenesis of malnutrition observed in this group of patients. It has been reported, that in vitro adipocytes exposed to acidotic medium decrease leptin secretion. The aim of present study was to analyze the possible impact of uraemic metabolic acidosis on leptinaemia in haemodialysis patients with chronic renal failure. - 94 haemodialysed patients (58 M, 36 F; mean age 45 +/- 1 years) were enrolled in this study. 56 patients were on haemodialysis treatment for one year using an acetate dialysis fluid, while 38 patients were haemodialysed at least for 3 months with a dialysate buffered with bicarbonate. Plasma leptin concentration, blood gases and body composition were assessed in all examined subjects. - Patients haemodialysed with an acetate and bicarbonate buffered dialysate did not differ with respect to body weight, body mass index (BMI), total fat mass (TFM) and plasma leptin concentration. Patients haemodialysed with an acetate buffered dialysate were characterized by a significantly more severe metabolic acidosis than patients on bicarbonate haemodialysis. Patients were divided according to the actual hydrogen ion concentration: over 60 nmol/l, 45-60 nmol/l and below 45 nmol/l. These subgroups did not differ significantly by body weight, BMI and TFM. Only a slightly (not significantly), lower median leptinaemia was found in patients with elevated hydrogen ion concentration. No significant correlation was noticed between blood hydrogen or hydrocarbonate ion concentration respectively and logarithmic values of plasma leptin concentration (tau = 0.025, p = 0.72; tau = - 0.021, p = 0.76 respectively). - From results obtained in this study we may conclude that, blood hydrogen ion concentration does not influence substantially or only moderately to plasma leptin concentration in haemodialysed patients.

Cobalt-activated acylase activity in experimental toxic liver damage.

Co++-activated acylase activity was studied in the blood serum and liver homogenates from rabbits poisoned with CCl4 in doses of 0-5 g/kg body weight intraperitoneally. Activity of this enzyme in serum increased on the first day after poisoning, but the rise was of short duration. Increased serum activity of the enzyme was accompanied by an increase in acylase activity in liver homogenates, which persisted to the ninth day, i.e. to the end of the observation period, when serum acylase activity returned to normal. Co++-activated acylase activity in serum was not correlated with its activity in liver homogenates. Co++-activated acylase activity was significantly correlated with AlAT and GGTP activities, but acylase and LAP were not correlated.

Prolactin secretion in patients with acute renal failure.

In 44 patients with acute renal failure serum prolactin levels were estimated using chloropromazine as a stimulant and alfa-bromocriptine as an inhibitory agent. Significantly elevated basal serum prolactin levels were found both in oliguric and polyuric patients with ARF. Intramuscular (i.m.) administration of chloropromazine markedly increased serum prolactin concentrations. In patients with ARF the apparent half life of prolactin, calculated from the prolactin curve obtained after alfa-bromocriptine administration, was moderately longer than in normals. From the results obtained the following conclusions were drawn: 1. Hyperprolactinemia of patients with ARF seems to be due predominantly to hypersecretion of this hormone and, to a lesser degree, to impair renal biodegradation. 2. In patients with ARF prolactin secretion is hyperresponsive to intramuscularly administered chloropromazine.

Concentration of 25-hydroxyvitamin D in serum of infants under the intermittent high-dose vitamin D3 prophylactic treatment.

The concentration of 25-hydroxyvitamin D was measured in serum of 90 healthy and 123 sick infants. The mean concentration of 25-OH-D in the group of healthy infants given intermittent prophylactic doses of vitamin D3 was 44.0 microgram/l and was nearly three times higher than the average concentration in healthy adults not given any vitamin D substitution. In the 123 clinically treated infants the average 25-OH-D concentration was 86.2 microgram/l, and 59.4% of infants had values over 40 microgram/l. In the subgroup of infants admitted to the hospital because of diarrhea, lower values were found than the average ones of clinically-treated infants. Two children with clinical rickets had very low 25-OH-D concentrations. The 25-OH-D half life in serum of infants varied from 19 to 27 days and single dose--300,000 IU (7.5 mg) of vitamin D3 was found to assure a sufficient 25-OH-D concentration in serum for as many as 190 days. It is concluded that high intermittent oral doses of vitamin D3 give an effective protection against rickets but at the cost of several times higher 25-OH-D concentration in serum and at the risk of hypervitaminosis D in some healthy infants.

Concentrations of leptin and neuropeptide Y in maternal plasma, umbilical cord blood and in amniotic fluid in pregnant women with EPH-gestosis.

Leptin is presumed to be related to body mass index (BMI) and body fat stores and is involved together with neuropeptid Y (NPY) in the regulation of appetite. As pregnancy is accompanied both by changes of BMI and appetite, performance of studies presented in this paper were fully justified. In 43 healthy pregnant women and in 18 pregnant women with mild or moderate EPH-gestosis, concentrations of leptin and NPY were estimated in maternal venous blood, umbilical cord blood and in amniotic fluid. The control group consisted of 26 healthy nonpregnant women. Healthy nonpregnant women showed a BMI of 23.08+/-0.65 kg/m2 which was significantly lower than in healthy pregnant women (26.9+/-0.4 kg/m2, p < 0.001) and in women with EPH-gestosis (29.7+/-0.9, p < 0.0001). Also in healthy pregnant women the BMI was significantly lower than in EPH-gestosis subjects (p < 0.001). In healthy nonpregnant women plasma leptin levels were significantly lower than in healthy pregnant and EPH-gestosis women (10.9+/-1.68 vs 14.99+/-1.28 vs 21.89+/-2.58 ng/ml, respectively). In umbilical cord blood plasma leptin levels were significantly lower than in maternal blood only in healthy pregnant women (7.37+/-0.69 vs 14.99+/-1.28 ng/ml) but not in EPH-gestosis subjects (18.06+/-3.38 vs 21.89+/-2.58 ng/ml). Leptin levels in amniotic fluid were significantly lower than in umbilical cord blood both in healthy pregnant women (2.25+/-0.20 vs 7.37+/-0.69 ng/ml) and EPH-gestosis women (6.58+/-2.62 vs 18.06+/-3.38 ng/ml). In EPH-gestosis women leptin levels were significantly higher than in healthy pregnant women in maternal blood (21.89+/-2.58 vs 14.99+/-1.28 ng/ml), umbilical cord blood (18.06+/-3.38 vs 7.37+/-0.69 ng/ml) and amniotic fluid (6.58+/-2.62 vs 2.25+/-0.2 ng/ml). In both examined pregnant groups plasma NPY levels were nonsignificantly lower in healthy pregnant and EPH-gestosis women (42.28+/-4.09 and 43.68+/-8.45 pg/ml, respectively) than in nonpregnant women 50.65+/-6.13 pg/ml). In normal pregnancy a significantly higher NPY level was found in umbilical cord blood as compared with respective values in EPH-gestosis women (116.28+/-17.0 vs 49.65+/-7.01 pg/ml). Finally in both examined groups of pregnant women the amniotic fluid NPY level was of similar magnitude (13.85+/-1.52 and 13.89+/-2.46 pg/ml in healthy pregnant and EPH-gestosis women respectively). No significant correlation was found between fetal birth weight and cord-serum leptin and NPY levels respectively.

Alterations of Tamm-Horsfall protein immunoreactivity after partial desialylation and deglycosylation.

The role of the carbohydrate moiety of Tamm-Horsfall protein (THP) was investigated by studying the effect of partial enzymatic desialylation and deglycosylation on its immunoreactivity. In our experiments primarily sialic acid alpha 2,6 linked to a galactose was split off, resulting in a 14% increase of immunoreactivity. It was increased up to 21% by further removal of the sugar residues. We also found that complexes composed of THP and human serum albumin, immunoglobulin G or transferrin reacted with anti-THP antibodies. When these complexes were formed with desialylated or deglycosylated THP an essential increase of this reactivity (about 25%) occurred. Our studies indicate that modifications of the carbohydrate moiety of THP (which might occur in vivo by changes in the glycosylation process e.g. in pathologic conditions) lead to increased exposure of THP to the immune system.

The nonselective adenosine antagonist theophylline does prevent renal dysfunction induced by radiographic contrast agents.

Radiocontrast agents (RCA) induce nephrotoxicity characterized by acute renal failure (ARF), which seems to be mediated partly by adenosine. ARF significantly influences erythropoietin (EPO) secretion and plasma renin activity (PRA). The present study assessed the influence of theophylline, a nonspecific adenosine receptor antagonist, on renal function, EPO secretion and PRA after the use of RCA. Fifty-eight patients underwent X-ray examinations with administration of RCA. Patients were randomized to receive either 165 mg of theophylline or placebo (saline) before the injection of 40 ml of high-osmolar contrast medium Plasma concentrations of EPO and PRA were assayed in blood samples drawn 2 hours before and 3, 6, 12 and 24 hours after RCA. Glomerular filtration rate, evaluated from endogenous creatinine clearance, urinary excretion of beta 2-microglobulin (beta 2-M), Tamm-Horsfall protein (THP) and albumin were assessed one day before RCA, on the day of RCA injection and one day later. In patients not treated with theophylline, RCA injection was followed by a significant reduction of GFR and increased urinary excretion of both beta 2-M and THP, which declined or were normal one day later. Simultaneously there was a significant decrease of plasma EPO and PRA. Theophylline prevented the decline of GFR, the increase of urinary beta 2-M and THP and the reduction of plasma EPO and PRA. The drug did not influence urinary albumin excretion. We conclude that RCA-induced impairment of renal excretory, endocrine and tubular function can be prevented by giving theophylline before RCA. These results suggest that adenosine may play a role in the pathogenesis of RCA-induced nephropathy.

Plasma parathyroid hormone, phosphatemia and vitamin D receptor genotype: are they interrelated?

It is not clear how the rate of bone mineral loss and vitamin D receptor (VDR) Bsml polymorphism in hemodialysed patients are related. We therefore analysed the relationships between indices of calcium-phosphate metabolism in respect to VDR genotype in 180 hemodialysed patients. We measured plasma concentrations of calcium, phosphate, iPTH, 1,25(OH)2D3 and activity of the bone fraction of alkaline phosphatase on the day before dialysis. VDR genotype BB, Bb and bb were found in 39, 84 and 57 patients, respectively. The allele frequency was B 0.45 and b 0.55. Subjects with BB genotype had insignificantly higher plasma levels of phosphate, iPTH and activity of the bone fraction of alkaline phosphatase, but significantly lower (p<0.02) concentrations of 1,25(OH)2D3 [iP (mmol/l): 2.05+/-0.09, 1.98+/-0.06, 1.93+/-0.06; iPTH (pg/ml): 257+/-50, 229+/-24, 219+/-30; AP(BF) (nmol/l/s): 515+/-45, 477+/-27, 457+/-34; 1,25(OH)2D3 (pg/ml): 23.4+/-1.5, 26.2+/-1.0, 29.3+/-1.3, for BB, Bb and bb respectively]. The strongest significant correlation between phosphatemia and iPTH was in the BB subgroup (r=0.343). Moreover, only in this subgroup did phosphatemia significantly contribute to the increase in iPTH, assessed by multiple regression analysis. In conclusion, it seems likely that BB VDR genotype in HD patients contributes to the severity of secondary hyperparathyroidism by a mechanism involving phosphatemia.

Biochemical monitoring of diabetic patients.

Tight metabolic control as assessed by estimation of glycated hemoglobin or albumin seems to be the main prophylactic factor in the prevention of most diabetic complications. By regular monitoring of the kidney size, GFR, and urinary albumin excretion, detection of early (reversible) diabetic nephropathy is possible. By appropriate dietary (protein restriction) and pharmacological (ACEI, antihypertensive drugs) treatment development of overt diabetic nephropathy may be prevented or markedly slowed.

Do opioid receptors participate in the regulation of atrial natriuretic peptide (ANP) secretion in hypertensive patients?

Experimental and clinical studies seem to prove that both endogenous opioids and atrial natriuretic peptide (ANP) are involved in blood pressure regulation. This raised the question, whether these two factors are functionally interrelated to each other. We tried to answer this question by assessing plasma ANP levels in 15 patients with II degrees essential hypertension and in 15 healthy subjects under water immersion (WI) conditions. In all subjects two WI tests were performed--one without pretreatment with naloxone, and a second one after blockade of opioid receptors by this opioid receptor antagonist. Parallel to ANP, plasma renin activity (PRA), aldosterone (ALD) and vasopressin (AVP) were assessed. In hypertensive patients significantly higher basal plasma ANP levels were found than in control subjects. WI induced a significant increase of plasma ANP in both examined groups which became markedly reduced after blockade of opioid receptors by naloxone. Naloxone did not influence the WI induced decrease of PRA, ALD and AVP respectively. From results presented in this study we conclude, that a.) opioid receptors seem to influence regulation of ANP secretion both in healthy normotensive subjects and patients with essential hypertension, and b.) that WI induced alterations of ANP on the one side and of PRA, ALD and AVP on the other side are not interrelated.

Influence of naloxone on prolactin secretion in patients with acute and chronic renal failure.

The influence of the opiate antagonist naloxone on chlorpromazine induced prolactin secretion was examined in 12 patients with acute renal failure (ARF), 12 patients with chronic renal failure (CRF) and in 12 healthy subjects. In all examined groups naloxone showed a suppressive effect on chlorpromazine induced prolactin secretion, which was more accentuated in normals and patients with ARF then with CRF. The results of these investigations suggest that endogenous opiates may be of importance in the regulation of prolactin secretion both in normals and uremic patients.

Influence of erythropoietin treatment on function of the pituitary-adrenal axis and somatotropin secretion in hemodialyzed patients.

In five hemodialyzed patients the influence of erythropoietin (EPO) treatment for 3 months on function of the pituitary-adrenal feedback and STH secretion was studied. Results were compared with those obtained in 6 hemodialyzed patients (No-EPO group) showing a comparable Hb concentration and Hct value as patients in the EPO group post-treatment and in 15 healthy subjects. EPO treatment was followed by a significant (ACTH and STH) or moderate (cortisol) suppression of basal plasma levels of ACTH, STH and cortisol respectively, and by a significant reduction of the response of plasma concentrations of these hormones to insulin-induced hypoglycemia. As the response of plasma levels of ACTH, STH and cortisol respectively in patients of the EPO group post-treatment differed markedly from that of the No-EPO group with similar Hb and Hct values, it seems that the EPO-induced endocrine alterations are not, at least not exclusively, a consequence of the improvement of anemia. Results presented in this study suggest that EPO treatment influences directly or indirectly the function of endocrine organs.