dinoprost and Nephritis

ANG II promotes inflammation through nuclear factor-kappaB (NF-kappaB)-mediated induction of cytokines and reactive oxygen species (ROS). The aim of the present study was to examine the effect of tetradecylthioacetic acid (TTA), a modified fatty acid, on NF-kappaB, proinflammatory markers, ROS, and nitric oxide (NO) production in two-kidney, one-clip (2K1C) hypertension. The 2K1C TTA-treated group had lower blood pressure (128 +/- 3 mmHg) compared with 2K1C nontreated (178 +/- 5 mmHg, P < 0.001). The p50 and p65 subunits of NF-kappaB were higher in the clipped kidney (0.44 +/- 0.01 and 0.22 +/- 0.01, respectively) compared with controls (0.25 +/- 0.03 and 0.12 +/- 0.02, respectively, P < 0.001). In the 2K1C TTA-treated group, these values were similar to control levels. The same pattern of response was seen in the nonclipped kidney. In 2K1C hypertension, cytokines plasma were higher than in control: TNF-alpha was 13.5 +/- 2 pg/ml (P < 0.03), IL-1beta was 58.8 +/- 10 pg/ml (P = 0.003), IL-6 was 210 +/- 33 pg/ml (P < 0.001), and monocyte chemoattractant protein-1 was 429 +/- 21 pg/ml (P = 0.04). In the 2K1C TTA-treated group, these values were similar to controls, and the same pattern was seen in the clipped kidney. Clipping increased 8-iso-PGF-2alpha (P < 0.01) and decreased NO production (P < 0.01 vs. control) in the urine. TTA treatment normalized these values. NO production was also lower in clipped and nonclipped kidney (P < 0.001). After TTA treatment, these values were similar to controls. The results indicate that TTA has a potent anti-inflammatory effect in 2K1C by inhibition of p50/p65 NF-kappaB subunit activation, reduction of cytokines production and ROS, and enhanced NO production.

Topics: Animals; Body Weight; Chemokine CCL2; Dinoprost; Disease Models, Animal; Eating; Free Radical Scavengers; Hypertension, Renal; Interleukin-1beta; Interleukin-6; Kidney Cortex; Male; Nephritis; NF-kappa B p50 Subunit; Nitrates; Nitric Oxide; Nitrites; Rats; Rats, Wistar; Reactive Oxygen Species; Sodium, Dietary; Sulfides; Surgical Instruments; Transcription Factor RelA; Tumor Necrosis Factor-alpha

The patients suffering from hypertonic nephritis were examined for renal hemodynamics, the activity of the renin-angiotensin-aldosterone system (RAAS), excretion of PGE2 and PGF2 alpha, and for a number of the parameters of water-electrolyte homeostasis. In A series, the patients suffering from latent and hypertonic nephritis (n = 11 in each group) were compared. In B series, two groups of the patients (n = 13 in each group) suffering from hypertonic nephritis associated with moderate or grave arterial hypertension were compared. The patients under comparison belonging to A and B series did not differ as regards the sex, age, nephritis standing, serum creatinine or proteinuria. As compared with the patients suffering from latent nephritis (A series), the patients with hypertonic nephritis showed a lower effective renal plasma flow, a greater resistance of the renal vessels, lesser PGE2 secretion, and a higher serum sodium concentration. As compared with the patients suffering from moderate hypertension (B series), the patients with associated hypertonic nephritis and grave hypertension demonstrated a higher resistance of the renal vessels, a higher activity of plasma renin, a larger concentration of plasma aldosterone and its excretion with urine, as well as a greater volume of the circulating blood. It is assumed that the development of arterial hypertension associated with hypertonic nephritis may be caused by renal hemodynamics deterioration, by relative activation of the renin-angiotensin system, inhibition of the depressor prostaglandin system and sodium retention. The progression of hypertension may be related to further deterioration of renal hemodynamics attended by RAAS activation and hypervolemia.

Topics: Creatinine; Dinoprost; Dinoprostone; Female; Hemodynamics; Humans; Hypertension; Hypertension, Renal; Male; Nephritis; Proteinuria; Renin-Angiotensin System; Water-Electrolyte Balance

The effects of prostaglandins E2 and F2 alpha on renal lesions induced by an anti-rat serum were investigated in rats. It was found that these prostaglandins, administered concomitantly with the antiserum, were able to prevent or remarkably attenuate these lesions. A very interesting finding is that, after prostaglandin administration, no or insignificant morphological alterations of the kidney occurred, in spite of the fact that its mononuclear cell infiltration was somewhat persistent. Hence, in addition to the known effects of these prostaglandins on the immune response components, the blockade of cellular receptors for immunoglobulins is to be considered as a main mechanism in explaining their preventive action in allergic nephritis.

Topics: Animals; Blood Proteins; Dinoprost; Dinoprostone; Female; Hypersensitivity; Immune Sera; Male; Nephritis; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains

The authors studied the effect of indomethacin and naproxen on the changes of renal prostaglandin E and F2 alpha concentration in experimental kidney infection, as well as the action of arginine-vasopressin in healthy rats. Naproxen proved to be an effective inhibitor of prostaglandin synthesis, as did indomethacin. In control animals an increased prostaglandin E and F2 alpha synthesis was observed caused by arginine vasopressin. It is supposed that ADH--depending on its concentration--has a metabolic modulator role in prostaglandin synthesis, which raises the possibility of a self-regulatory mechanism of water reabsorption.

Topics: Animals; Arginine Vasopressin; Deamino Arginine Vasopressin; Dinoprost; Escherichia coli Infections; Female; Indomethacin; Kidney; Naproxen; Nephritis; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains

An accelerated model of nephrotoxic serum nephritis (NTN) was induced in two groups of Sprague-Dawley rats on the following regimens: (a) a diet deficient in essential fatty acids that contained 20% coconut oil (rats A); (b) a diet supplemented with essential fatty acids that contained 20% safflower oil (rats B). Animals from both groups developed a severe proteinuria reaching its maximum 4 days after the injection of nephrotoxic serum (NTS). Kidney tissue was studied by light and immunofluorescent microscopy 2 to 21 days after NTS injection. The glomeruli of rats A exhibited much more fibrinoid deposition than did those of rats B. A comparable glomerular infiltration by mononuclear cells was observed in both groups of animals between the 2nd and 5th day following the injection of NTS. The number of intrinsic glomerular cells incorporating 3H-thymidine in vivo, however, was significantly lower in rats A than it was in rats B. The outgrowth capacity of glomerular cells in vitro was significantly lower in glomerular explants from rats A than it was in glomerular explants from rats B. These findings demonstrate that, in this model of rat NTN, a diet deficient in essential fatty acids has no major effects on the course of the disease during the first 3 weeks following NTS injection. They further show that the proliferation of intrinsic glomerular cells can be modulated by altering prostaglandin metabolism.

Topics: Animals; Cell Division; Diet; Dinoprost; Dinoprostone; Fatty Acids, Essential; Female; Glomerulonephritis; In Vitro Techniques; Kidney Glomerulus; Nephritis; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains

Topics: Adolescent; Adult; Alprostadil; Chronic Disease; Cyclic AMP; Diagnosis, Differential; Dinoprost; Female; Humans; Male; Medicine, Chinese Traditional; Medicine, East Asian Traditional; Middle Aged; Nephritis; Prostaglandins E; Prostaglandins F