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Biomedical subjects

M Rathaus

Publications and source records attributed to M Rathaus.

At least 55 records · Page 3Linked to original sources
PubMed1988

Role of glomerular prostanoid in control of glomerular filtration rate in rats.

It is generally accepted that the main action of glomerular prostanoids (GPs) on glomerular filtration rate (GFR) is to modulate the activity of different vasoconstrictors, specially in states of renal hypoperfusion. However it was also suggested that GPs may directly affect GFR. The present study was focused on this last hypothesis, in different experimental models, in rats. In adriamycin induced acute renal failure, the transient decrease of GFR is associated with higher levels of thromboxane B2. Later on, when GFR returns to normal, vasodilator prostaglandins synthesis was also increased. In captopril induced renal failure in Na depleted rats (where GPs synthesis remained normal), stimulation of PGE2 and PGI2 production by K and NaCl was associated with a significant improvement of GFR. Furthermore, the increase in GFR induced by NaCl was prevented by inhibition of prostaglandin synthesis. Infusion of atrial natriuretic peptide in euvolemic rats induce a marked elevation both of GFR and PGE2 synthesis. It was abolished by previous administration of prostaglandin synthesis inhibitor. In conclusion, glomerular prostanoids may influence GFR, either directly, or as mediator or modulator of other vasoactive hormones.

Acute Kidney Injury↗
PubMed1988

Atrial natriuretic peptide administration to normal and salt depleted rats--effects on digoxin-like immunoreactive factor, aldosterone, ACTH, and renal function.

In view of the known interrelationships between renin, aldosterone, and atrial natriuretic peptide (ANP), we sought to examine whether there also exists an interaction between ANP and digoxin-like immunoreactive factor (DLIF). We therefore studied the effects of ANP administration on normal and salt-depleted rats, and measured the effects on blood pressure, urine output, glomerular filtration rate, sodium excretion, aldosterone, ACTH, and DLIF levels. ANP administration resulted in a significant elevation of sodium excretion and glomerular filtration rate and a fall in blood pressure. DLIF concentrations in plasma rose significantly, as did urinary DLIF excretion. ANP administration resulted in a fall in aldosterone as well as ACTH. These observations suggest that ANP has a direct inhibitory effect on ACTH secretion. Our findings support the concept of an interrelationship between ANP and DLIF.

Adrenocorticotropic Hormone↗
PubMed1988

Prostanoids in renal failure induced by converting enzyme inhibition in sodium-depleted rats.

Clearances of inulin (CIn) and p-aminohippurate (CPAH) were measured in four groups of rats before and after intravenous administration of acetylsalicylic acid (ASA): 1) controls, on normal Na intake, 2) captopril-treated (30 mg.kg-1.day-1) on normal Na intake, 3) Na depleted, and 4) Na depleted, captopril-treated. In Na-depleted animals, CIn and CPAH were similar to controls but decreased significantly with ASA. In Na-depleted, captopril-treated rats, CPAH was slightly decreased, but CIn was significantly reduced (P less than 0.01). Both were not affected by ASA. Urine output was unchanged and the kidneys appeared normal on histological examination. The production of prostaglandins E2 (PGE2), F2 alpha (PGF2 alpha), and thromboxane B2 (TxB2) was measured in isolated glomeruli, cortical tubule suspensions, and medullary and papillary slices. Captopril increased PGE2 production by glomeruli and PGF2 alpha and TxB2 synthesis in papillary slices. Na depletion selectively enhanced the production of PGE2 by glomeruli and papillae. In contrast, the synthesis of prostanoids was significantly decreased in captopril-treated, Na-depleted rats. These findings suggest that in this model, functional nonoliguric renal failure may be related to abnormalities of prostanoid synthesis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Effects of sodium loading on the renal synthesis of prostanoids in the rat.

1. The production of prostaglandin (PG) E2, F2 alpha and thromboxane B2 (TXB2) by isolated glomeruli, cortical tubular suspensions and medullary and papillary slices was measured in normal Long-Evans rats 4, 8 and 14 days after starting on oral Na+ load and the results were compared with those of rats on a normal Na+ intake. 2. In glomeruli, PGE2 decreased at days 4 and 8, and returned to normal at 14 days. PGF2 alpha decreased only at day 4 and TXB2 decreased in all Na+-loaded animals. In cortical suspensions, a transient decrease of PGE2 was observed at day 4. In medullary slices, PGE2 and TXB2 decreased in all experimental periods. In contrast, in papillae, a significant increase of PGE2 was observed with Na+ loading at day 8, but PGF2 alpha and TXB2 did not change consistently. 3. Similar changes were observed in rats with hypothalamic diabetes insipidus (DI rats) Na+ loaded for 4 days, as compared with DI rats on a normal Na+ intake. 4. The results suggest that prostanoids participate in the renal adaptation to an increased Na+ intake, and that this response is relatively independent of the presence of antidiuretic hormone.

Animals↗
PubMed1986

NADH-dependent prostaglandin E2-9-ketoreductase activity and prostaglandin synthesis in the Brattleboro rat kidney: effects of the antidiuretic hormone.

The activity of prostaglandin (PG)E2-9-ketoreductase (9KR), an enzyme catalyzing the conversion of PGE2 to PGF2 alpha, was significantly increased in glomerular and cortical homogenates of diabetes insipidus (DI) rats, as compared to normal Long Evans (LE) rats, and did not change with ADH treatment. Medullary 9KR was similar in the three groups and papillary 9KR was increased, but not significantly, in both groups of DI rats. Km values for PGE2 and NADH were compared in the various compartments of the kidney. Levels of 9KR were not correlated with the PGE/PGF ratio in urine or supernatants. The synthesis of PGE2 and PGF2 alpha by isolated glomeruli was increased in DI rats. This was not reversed by ADH treatment, PGE2 synthesis increasing even further, especially in the presence of arachidonic acid. In contrast, medullary slices produced significantly less PGs in DI than in LE rats and returned to normal with ADH treatment. Papillary slices produced similar quantities of prostaglandins in all groups. The results do not support the concept that the alterations in PG synthesis observed in DI rat are related only to changes in 9KR activity, but do not exclude the possibility that the enzyme participates in the regulation of PG biosynthesis.

Animals↗
PubMed1986

Sodium intake as a determinant of urinary prostaglandin excretion. Studies in the Brattleboro rat.

In order to investigate the effects of changes in sodium (Na) balance on the renal production of prostaglandins (PG) E2 and F2 alpha in the absence of antidiuretic hormone (ADH), studies were performed in Brattleboro rats, without endogenous ADH, and in heterozygote Long Evans rats which served as controls. All rats received a diet virtually devoid of Na, with distilled water ad libitum, and Na intake was modified by adding different quantities of Na to the drinking water. Three groups were studied for each strain: normal Na intake, low Na intake and Na loading. At the end of a 14 day diet period, urinary PGE2 and PGF2 alpha were measured by radioimmunoassay in collections obtained for three consecutive days. In the Na depleted animals, both PGE2 and PGF2 alpha decreased. The PGE2/PGF2 alpha ratio (E/F ratio) was unchanged. In contrast, Na loading induced a significant decrease of PGE2 but PGF2 alpha increased, though not significantly. The E/F ratio was significantly decreased. The results were qualitatively similar in the presence or absence of ADH, but the Brattleboro rats, overall, excreted less PGs than controls. The results suggest that changes in Na balance are major factors influencing urinary PG excretion. These substances probably play a role in the modifications of Na handling by the kidney in different balance states.

Animals↗
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

Renal prostaglandins E2 and F2 alpha throughout normal human pregnancy.

Twenty-five normal pregnant women were studied sequentially at 4-week intervals, beginning from weeks 8-16 until delivery. In eighteen women the study was repeated 6 weeks after delivery. The 24-h urinary excretion of PGE2 and PGF2 alpha, plasma renin activity (PRA), plasma aldosterone and fractional excretion of sodium (FENa) were measured at each visit. PGE2 and PGF2 alpha increased progressively throughout pregnancy (867 +/- 81 and 1048 +/- 94 ng 24 h-1 respectively, before week 15 and 1581 +/- 175 and 2625 +/- 305 ng 24 h-1, respectively, after week 35) and returned to normal values 6 weeks after delivery (748 +/- 107 and 1503 +/- 165 ng 24 h-1, respectively). PRA and aldosterone increased in a similar fashion, but values of prostaglandins did not correlate with those of PRA or aldosterone. PGE2 correlated directly with FENa but this correlation was weak. These results may suggest that tubulo-interstitial prostaglandins play a role in the regulation of sodium homeostasis during pregnancy.

Adult↗
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

[Anemia in primary hyperparathyroidism].

Among the complications associated with primary hyperparathyroidism, anemia has not been extensively studied. In order to assess the frequency of this anemia we make a retrospective study of the medical records of 62 patients with a primary hyperparathyroidism. In 40 of the 62 hyperparathyroidic patients the diagnosis was surgically proven (group 1) and in 22, typical laboratory changes were found (group 2). In all these cases no other causes of anemia, except hyperparathyroidism, could be found. The 2 groups were similar concerning age and sex. A normochromicnormocytic anemia was present in 11 patients in group 1 (24,5%) and in 7 in group 2 (31, 8%). This anemia was corrected after a successfull parathyroidectomy (parathyroid adenoma in all the operated cases). Anemia was correlated with neither Ca and P blood levels nor C1/P ratio. A significant inverse correlation was found between age and hemoglobin in anemic hyperparathyroidic patients. The etiopathogeny of this findings is discussed.

Adenoma↗
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↗
PubMed1985

Effect of sodium loading on the urinary excretion of prostaglandins E2 and F2 alpha in rats with hereditary diabetes insipidus (Brattleboro rats).

Current evidence suggests that the antidiuretic hormone (ADH) and changes in sodium balance influence renal prostaglandins (PGs). To separate these two mechanisms, the effect of sodium loading on the urinary excretion of PGE2 and PGF2 alpha was studied in female Brattleboro rats with diabetes insipidus (DIHO) and compared with that in female, age matched, heterozygous Long Evans controls (LEHE). Ten DIHO and ten LEHE rats had a normal sodium intake. In ten DIHO rats a 0.16% NaCl solution was supplied instead of drinking water for either 8 days (n = 5) or 14 days (n = 5). In two groups of LEHE rats, sodium loading was obtained with a 0.80% NaCl solution for the same study periods. Urine PGs were measured by radioimmunoassay in three 24 h urine collections for each rat. Urine PGs were significantly increased in the 8 day loaded but not in the 14 day loaded LEHE rats. In DIHO rats, a non-significant increase in both PGE2 and PGF2 alpha was present after 8 days of sodium loading, while PGE2 and the E/F ratio were decreased after 14 days of salt loading. The findings suggest that the natriuresis induced by sodium loading in the rat may be mediated in part by increased production of PGs. In addition, it seems that ADH plays a role in this response.

Animals↗
PubMed1985

Urinary kallikrein in normal pregnancy, pregnancy with hypertension, and toxemia.

The 24-hour urinary excretion of kallikrein (K) and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 +/- 8.1 KU/24 h) and HP (106.5 +/- 8 KU/24 h) compared to NW (57 +/- 8.23 KU/24 h) (p less than 0.05). PGE2 excretion was decreased in EH (403.25 +/- 90.6 ng/24 h) compared to NW (508.6 +/- 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 +/- 93.2 ng/24 h in NP and significantly more in HP, 1,885 +/- 40 ng/24 h (p less than 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 +/- 6.1 KU/24 h) and PGE2 (583 +/- 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.

Adolescent↗
PubMed1985

Urinary prostaglandins E2 and F2 alpha in chronic renal failure. Influence of chronic and acute changes in Na balance.

The role played by renal prostaglandins E2 (PGE2) and F2 alpha (PGF 2 alpha) in the modification of sodium homeostasis in chronic renal failure (CFR) was studied. The 24-hour urinary excretion of PGE2 and PGF2 alpha was measured before and after 5 days of a diet containing less than 20 mmol/day of sodium in 6 patients with CRF. At the end of this period, an acute sodium load (77 mmol/h of NaCl for 4 h) was administered and prostaglandins measured in hourly urine collections. In contrast to the findings previously reported in normal subjects, PGE2 and PGF2 alpha decreased with the low-sodium diet. The ratio PGE2/PGF2 alpha (reflecting the activity of the enzyme PGE2-9-ketoreductase) was greatly increased and did not change with the low-sodium diet. The acute sodium load induced an increase in urinary prostaglandins. The results suggest that prostaglandins may contribute to natriuresis in CRF, under basal conditions, after a short-term sodium depletion and in response to an acute sodium load. The changes in prostaglandin excretion in CRF could be related to decreased activity of PGE2-9-ketoreductase.

Adult↗
PubMed1983

The urinary excretion of prostaglandins E2 and F2 alpha in essential hypertension.

The 24 h urinary excretions of prostaglandins E2 (E2/d) and F2 alpha (F2 alpha/d) were measured in twenty-five normal subjects and in thirty-five patients with essential hypertension [seventeen with low renin (LRH) and eighteen with normal renin (NRH) hypertension]. E2/d was lower in patients with LRH than in normal subjects (P less than 0.01), whereas no difference was found between patients with NRH and the controls. F2 alpha/d was similar in patients with LRH and in the normal subjects, but was significantly greater in patients with NRH (P less than 0.02). The ratio of prostaglandin E2 to prostaglandin F2 alpha was decreased in hypertensive patients (P less than 0.02), although in the NRH subgroup the difference was not statistically significant. It appears that LRH is associated with impaired production of prostaglandin E2, while a deranged relationship between the two prostaglandins exists in all the patients with essential hypertension. These changes in prostaglandin production could possibly contribute to the pathogenesis of hypertension, by increasing renal vascular resistance and decreasing sodium excretion. Alternatively, they might be a secondary phenomenon, reflecting changes in renal prostaglandin metabolism induced by the hypertensive state.

Adult↗