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E Podjarny

Publications and source records attributed to E Podjarny.

49 records · Page 3Linked to original sources
PubMed1986

Effect of angiotensin II on prostanoid synthesis in isolated rat glomeruli.

The influence of angiotensin II (ANG II) on the synthesis of glomerular prostanoids is controversial, possibly because of the different methodologies employed. In order to assess this inter-relationship isolated rat glomeruli were incubated with and without shaking. The use of shaking during incubation significantly increased the amounts of prostanoid synthesized, most probably because of continuous non-specific activation of phospholipase (PLA2) activity. After preincubation in a non-shaking bath, ANG II was added for a second incubation period. A marked increase of prostaglandin (PG) E2, and, to lesser degree, of thromboxane (TX) B2 was noted, with no change on PGF2 alpha synthesis. These results show (a) that preincubation without shaking, by lowering the non-specific activation of the PLA2 activity, may unmask, in vitro, specific peptide stimulation, and (b) that ANG II, stimulating principally PGE2 synthesis, may modify the vasoactive status of the glomerular vasculature.

Angiotensin II↗
PubMed1986

Effect of vasoactive agents on prostanoid synthesis in isolated rat glomeruli.

We studied the influence of vasoactive substances (angiotensin II, epinephrine, norepinephrine and acetylcholine) on the synthesis of prostanoids in isolated rat glomeruli. A significant increase of prostaglandin E2, and of thromboxane B2, but not of prostaglandin F2 alpha synthesis was observed after the administration of angiotensin II at physiological doses. Neither catecholamines nor acetylcholine influenced prostaglandin synthesis. The stimulation of vasoactive prostaglandins by angiotensin II, may modify the hemodynamic status of the glomerulus.

Acetylcholine↗
PubMed1986

High incidence of hypertension in older patients after unilateral nephrectomy. A retrospective study.

Twenty-six normotensive patients, who underwent unilateral nephrectomy for nontumoral urological diseases, were reevaluated. The mean postoperative follow-up period was 13.8 +/- 0.7 years. Eleven patients developed hypertension, and 15 patients remained normotensive. The former were 47.1 +/- 3.3 years old, and the latter 36.5 +/- 2.9 years old at the time of nephrectomy (P less than 0.02). The mean preoperative systolic blood pressure was higher in the group of 11 hypertensive patients (126.7 +/- 2.4 mm Hg) than in the 15 normotensive patients (118.2 +/- 2.9 mm Hg), P less than 0.04. Preoperative diastolic blood pressure was similar in the two groups (77.8 +/- 1.5 vs. 75 +/- 2 mm Hg). Preoperative and follow-up serum creatinine levels were similar in both groups. Mean creatinine clearance (Ccr) at the time of follow-up was not significantly different in the hypertensive patients compared with the normotensive patients. One patient developed proteinuria and chronic renal failure (Ccr of 31 ml/min). Two other patients with normal Ccr had a daily protein excretion of 840 and 2,000 mg/24 h, respectively. The incidence of hypertension, after nephrectomy, of 75% in patients greater than 55 years old seems to be significantly higher than the 30% reported in an aged-matched normal Israeli population. This did not apply to the patients less than 55 years old. In most of the cases, long-term follow-up did not reveal significant uninephrectomy induced changes in renal function.

Adult↗
PubMed1985

Effect of potassium loading on prostaglandin E2 and F2 alpha excretion in the Brattleboro rat.

In order to assess the relative roles played by potassium (K) and the antidiuretic hormone (ADH) on the renal production of prostaglandins (PG) E2 and F2 alpha, the 24 hour urinary excretion of these substances was measured in Brattleboro rats (devoid of ADH) and in control Long Evans heterozygote rats. Rats of each strain received either a normal K intake or a K load for 8 days. Urinary PGE2 and PGF2 alpha were measured by radioimmunoassay in three consecutive 24 h urine collections obtained after the above periods. K loading induced an increase in PGF2 alpha (p less than 0.01), PGE2 showing a non significant trend to decrease. The E/F ratio was decreased in K loaded animals. The changes were qualitatively similar in presence or absence of ADH, but animals with diabetes insipidus had lower levels of PGs than control animals. The results suggest the possibility that K loading induces an increase in the activity of the renal enzyme PGE2-9-ketoreductase. The resulting increase in PGF2 alpha could play a role in K excretion and this response is probably independent of ADH.

Animals↗
PubMed1984

Glomeruli cooperate with macrophages in converting arachidonic acid to prostaglandins and hydroxyeicosatetraenoic acids.

The interaction of proliferating macrophages with the glomerulus may play an important role in certain forms of glomerulonephritis. This interaction could involve metabolites of arachidonic acid (C20:4) such as prostaglandins (PG) and lipoxygenase products. We therefore investigated the conversion of exogenous [3H] C20:4 into hydroxyeicosatetraenoic acids (HETE) and PG by isolated glomeruli and macrophages from rats, alone and in combination. As demonstrated by HPLC, glomeruli converted C20:4 predominantly to lipoxygenase products -mainly 12-HETE- and, to a lesser extent, to PG. Resident macrophages converted C20:4 to equivalent amounts of HETE and PG, mainly 12-HETE and 6 keto-PGF1 alpha. When macrophages and glomeruli were studied in combination, a striking interaction was detected in both pathways of C20:4 metabolism. Production of 6 keto-PGF1 alpha was stimulated and considerable amounts of TXB2, PGD2 and hydroxyheptadecatrienoic acid (HHT) were also produced. Total 12-HETE production was unchanged. When a lipid extract of glomeruli, containing oxygenated metabolites of C20:4, was added to macrophages, stimulation of 12-HETE occurred without any change in HHT or PG formation. When, on the contrary, a lipid extract from macrophages was added to glomeruli, 12-HETE production by the glomeruli was nearly completely abolished. Thus the unchanged total 12-HETE production by coincubated glomeruli and macrophages resulted from its increased production by macrophages and its decreased production by glomeruli. These data suggest that interaction between glomeruli and macrophages results in activation of C20:4 metabolism by macrophages followed by inhibition of C20:4 metabolism by glomeruli. Such a regulatory process could play a role in the inflammatory response to immunological injuries during macrophage-dependent human and experimental glomerulonephritis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
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↗