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Biomedical subjects

M Rathaus

Publications and source records attributed to M Rathaus.

70 records · Page 4Linked to original sources
PubMed1983

Effect of atenolol treatment on urinary prostaglandins E2 and F2 alpha in essential hypertension.

The urinary excretion of prostaglandins (PG) E2 and F2 alpha was measured by radioimmunoassay in 15 patients with essential hypertension, before and after 2 and 4 weeks of treatment with the selective beta 1-adrenergic blocker, atenolol. Systolic and diastolic blood pressure, pulse rate and plasma renin activity decreased significantly during the treatment. No change was observed in renal function and electrolyte balance. The 24-hour excretion of PGE2 and PGF2 alpha was also unaffected by the antihypertensive treatment. The above findings, in contrast with those previously observed with another beta-blocker, propranolol, suggest that tubular beta-receptors are not involved in the synthesis of PGs. The different hemodynamic effects of the two drugs are the most likely explanation for the different responses in prostaglandin excretion.

Adult↗
PubMed1982

Effect of chronic and acute changes in sodium balance on the urinary excretion of prostaglandins E2 and F2 alpha in patients with essential hypertension.

The 24-hour urinary excretion of prostaglandins (PGs) E2 and F2 alpha, plasma renin activity (PRA), and aldosterone were measured in 7 normal subjects and 8 patients with essential hypertension before and after 5 days of a diet containing less than 20 mmol/day of sodium. Subsequently, sodium was infused intravenously for 4 h (77 mmol/h), and urinary PGs measured in hourly urine collections. Plasma renin activity and aldosterone were measured at hours 2 and 4. In the normal subjects, PGE2 increased significantly (p less than 0.0005), with the diet, while PGF2 alpha did not change. The E/F ratio was increased significantly (p less than 0.01). In contrast, in the hypertensive patients no changes were observed in PGs excretion or in the E/F ratio. PRA and aldosterone were in the normal range after the diet in 4 patients and low in the other 4. Apart from PRA and aldosterone levels, there were no differences between these two subgroups of patients, with regard to change in body weight, blood pressure or electrolyte excretion. PG excretions were also similar. With the Na infusion, PGs returned to control values in the normal subjects. In the hypertensive patients, PG excretion decreased to almost undetectable levels. This coincided with the phenomenon of exaggerated natriuresis. It is concluded that: (1) in hypertensive subjects PGs synthesis is not influenced by chronic changes in the volume status, and (2) renin secretion is relatively independent of PG production in the hypertensive subjects. We suggest that the changes in PG synthesis in hypertension are possibly related to altered sodium handling by the hypertensive kidney.

Adult↗
PubMed1982

Increased renal prostaglandins in normal pregnancy and in pregnancy with hypertension.

The 24-hour urinary excretion of prostaglandins (PGs) E2 and F2 alpha (which reflects the renal synthesis of these substances) was measured by radioimmunoassay in normal nonpregnant women (NW, n = 23), nonpregnant women suffering from essential hypertension (HW, n = 23), normal pregnant women (NP, n = 24) and women with hypertension in pregnancy (HP, n = 14). All pregnant women were in the third trimester of their pregnancy (week 24-40). The excretion of both PGE2 and PGF2 alpha was increased in NP as compared to NW. PGF2 alpha was relatively more elevated, leading to a decreased PGE2/PGF2 alpha ratio. In HP, PGE2 and PGF2 alpha excretions were even greater, and the PGE2/PGF2 alpha ratio was even lower than in NP. This contrasted with the lowered PGE2 excretion in HW. The increased renal PGs synthesis in normal pregnancy could be related to the effects on the kidney of several hormonal changes peculiar to pregnancy. In addition, the lowered PGE2/PGF2 alpha ratio suggests the possibility of an increased activity of the PGE2-9-ketoreductase, which could be related to the changes in renal sodium handling observed in pregnancy. The pattern of PGE2 excretion in HP is opposite to that observed in HW (i.e. increase rather than decrease). However, both groups share the lowered PGE2/PGF2 alpha ratio with respect to the normotensive counterparts. The causes of altered PG synthesis in pregnant women with hypertension are presently unclear.

Adult↗
PubMed1982

Effect of propranolol treatment on the urinary excretion of prostaglandins E2 and F2 alpha in patients with essential hypertension.

The 24-h urinary excretion of prostaglandins (PG) E2 and F2 alpha, which reflects the renal synthesis of these substances, was measured by radioimmunoassay in 10 patients with essential hypertension before and after treatment with propranolol. In addition, changes in the urinary excretion of PGE2 and PGF2 alpha after furosemide injection were also studied before and after propranolol treatment. The urinary excretion of PGE2 was significantly increased after propranolol treatment, whereas that of PGF2 alpha did not change. An enhanced response in PGE2 excretion after furosemide injection was observed after propranolol treatment. In contrast PGF2 alpha increased in response to furosemide before, but not after, propranolol treatment. Changes in renal hemodynamics induced by propranolol seem to be the main factor in PGE2 alpha increase. However, an indirect effect of beta-blockade or a direct effect on the enzymes governing renal PG synthesis cannot be ruled out.

Adult↗
PubMed1981

Effect of chronic and acute changes in sodium balance on the urinary excretion of prostaglandins E2 and F2 alpha in normal man.

1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2 alpha was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing less than 20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion. 2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 +/- 201.6 SEM to 1761.3 +/- 304.9 ng/24 h, P less than 0.0005). Prostaglandin F2 alpha also increased from 1187.0 +/- 390.1 to 1435.6 +/- 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2 alpha ratio increased from 0.83 +/- 0.2 to 1.52 +/- 0.34 (P less than 0.01). Plasma renin activity and aldosterone rose significantly (P less than 0.05 and less than 0.0025 respectively). 3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 +/- 29.9 to 86.7 +/- 22.9 ng/h (P less than 0.05) and to 36.9 +/- 5.96 ng/h after 4 h. Prostaglandin F2 alpha decreased at a slower rate, from 98.4 +/- 18.7 to 37.5 +/- 8.8 ng/h at 4 h (P less than 0.02). At 4 h the prostaglandin E2/prostaglandin F2 alpha ratio returned to control values (0.90 +/- 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P less than 0.02 and less than 0.0025 respectively) and reached control values after 4 h. 4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2 alpha and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E1 9-keto-reductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.

Adult↗
PubMed1981

Is anemia of chronic renal failure related to secondary hyperparathyroidism?

A pathogenetic role of secondary hyperparathyroidism in the anemia of chronic renal failure has been suggested. To investigate this relationship, the biochemical factors of secondary hyperparathyroidism (calcium, phosphorus, alkaline phosphatase, and immunoreactive parathyroid hormone) were correlated with hematocrit levels in 96 long-term hemodialysis patients. We also compared hematocrit values before and after parathyroidectomy in 18 patients. No correlation between hematocrit level and biochemical indices of secondary hyperparathyroidism could be found. However, in 44% of the patients with parathyroidectomies, the hematocrit reading increased after surgery. The importance and possible cause of this improvement of anemia in this group is discussed.

Adolescent↗
PubMed1980

Minimal-change nephropathy and malignant thymoma.

A 56-year-old man had fever, precordial pain, and a mediastinal mass. The mass disappeared two months later and the patient remained asymptomatic for 2 1/2 years. At that time a full-blown nephrotic syndrome developed, with minimal-change glomerulopathy. The chest x-ray film showed the reappearance of a giant mediastinal mass. On biopsy of the mass, malignant thymoma was diagnosed. Association between minimal-change disease and Hodgkin's disease is well known, while the association with malignant thymoma has not been previously reported. The relationship between malignant thymoma and minimal-change disease is discussed, and a possible pathogenic mechanism involving cell-mediated immunity is proposed.

Humans↗
PubMed1980

Effect of furosemide on renal prostaglandins E2 and F2 alpha in normal subjects and in patients with essential hypertension.

The urinary excretion of prostaglandins (PG) E2 and F2 alpha, which reflects the renal synthesis of these substances, was evaluated by radioimmunoassay before and after an i.v. injection of furosemide in 10 normal subjects and in 10 patients with essential hypertension. In most normal subjects, urinary PGE2 increased after furosemide injection, whereas PGF2 alpha decreased to undetectable levels. In the hypertensive subjects, PGE2 increased to a lesser degree or decreased, but PGF2 alpha excretion was unchanged or augmented. These results suggest that furosemide may increase PGE2 synthesis not only by increasing the availability of the substrate arachidonic acid or by inhibiting the action of the catabolizing enzyme 15-hydroxyl-PG-dehydrogenase, as has been proposed, but also by depressing the activity of the enzyme PGE2-9-ketoreductase, which catalyzes the conversion of PGE2 to PGF2 alpha. In essential hypertension, an increased activity of PGE2-9-ketoreductase could explain the decreased levels of PGE2 that have recently been described in these patients. Whether these abnormalities in PG interconversion play a role in the pathogenesis of the hypertensive state or are secondary to it remains a question for further investigation.

Adult↗
PubMed1979

[Leiomyoma of the small bowel with hypercalcaemia: presence of a substance with parathormone activity (author's transl)].

A leiomyoma of the small bowel produced laboratory features of hyperparathyroidism which disappeared promptly after tumour resection. Hypercalcaemia, hypophosphatemia, hyperchloremia, elevated chloride/phosphorus ratio, increased urinary cyclic AMP, and blood levels of immunoreactive parathormone were present. Electron microscopy showed dense round granules in the tumour cells.

Aged↗
PubMed1979

Anemia and secondary hyperparathyroidism in chronically hemodialyzed patients.

A role in the pathogenesis of the anemia of chronic renal failure has been attributed to secondary hyperparathyroidism. An amelioration of anemia after subtotal parathyroidectomy has been described. In the present study, no correlation was found between the severity of anemia and the level of serum parathormone in dialyzed patients. Furthermore, in seven patients, no improvement of the anemia was observed after parathyroidectomy.

Adolescent↗