Copper and zinc metabolism in aminonucleoside-induced nephrotic syndrome.

Copper (Cu) and zinc (Zn) were measured in urine, serum and tissues from rats with nephrotic syndrome (NS) induced with a single subcutaneous dose of puromycin aminonucleoside (PAN; 15 mg/100 g BW). Control animals were pair-fed. Urine was collected daily, and the rats were sacrificed on day 10.

Abnormalities of coagulation in experimental nephrotic syndrome.

The human nephrotic syndrome is accompanied by important alterations of the coagulation system related proteins. The purpose of the present study was to examine the activity of coagulation- and fibrinolysis-related proteins in plasma and urine of control and puromycin aminonucleoside injected rats on days 2 (prenephrotic stage) and 10 (nephrotic stage). We measured the prothrombin time (PT), the activated partial thromboplastin time (aPTT), and the activities of (1) the coagulation factors (CFs) I, II, V, and VII-XII; (2) the inhibitor of coagulation antithrombin III (ATIII), and (3) the component of the fibrinolytic system alpha 2-antiplasmin (alpha 2-APL).

Angiotensin II and catecholamines interaction in short-term low protein feeding.

Renal and systemic hemodynamic responses to an alpha-adrenergic agonist (norepinephrine, NE) and an alpha-adrenergic antagonist (phentolamine, PHEN) were studied in weanling rats pair-fed isocaloric diets containing either normal (NP, 23%) or low (LP, 6%) protein. Mean arterial pressure (MAP) rose less with NE and fell more with PHEN in LP than in NP. Plasma NE and epinephrine (E; 46 +/- 5 and 51 +/- 4 ng/ml) were higher in LP than in NP (26 +/- 3 and 39 +/- 3 ng/ml).

Angiotensin I-converting enzyme activity in rats with carbon tetrachloride-induced acute renal failure.

The angiotensin I-converting enzyme (ACE) activity was measured in urine, serum, and tissues from rats with carbon tetrachloride (CCl4)-induced acute renal failure on days 1, 2, 3, and 7 after CCl4 administration. Serum ACE increased on days 1 to 3. Heart, lung, small intestine, brain, and testis ACE decreased, whereas kidney and liver ACE remained unchanged.

Mechanisms involved in the progression to glomerular sclerosis induced by systemic hypertension during mild puromycin aminonucleoside nephrosis.

To evaluate the contribution of systemic hypertension in the progression of nephropathies to glomerular sclerosis, a mild form of puromycin aminonucleoside (PAN) nephrosis was associated with Goldblatt hypertension and studied after 18 weeks. We studied four groups: Group I, controls; Group II, Goldblatt hypertension; Group III, PAN nephrosis; and Group IV, both conditions. Systolic blood pressure, 24-h proteinuria, serum cholesterol, triglycerides, glomerular hemodynamics, and histological studies were compared among the groups.

Effect of captopril on urinary excretion of renin and angiotensinogen in aminonucleoside nephrosis.

Puromycin aminonucleoside (PAN)-nephrotic rats show high plasma renin, low plasma angiotensinogen (Angt), and increased urinary excretion of renin and Angt. In this work, we studied the effect of captopril on urinary excretion of total protein, renin, and Angt for 25 days after PAN injection. Captopril had no effect on total protein urinary excretion; however, captopril did enhance the urinary excretion of renin and did decrease the urinary excretion of Angt.

Activity of serum enzymes in puromycin aminonucleoside-induced nephrotic syndrome.

Total serum protein, serum albumin, total urine protein excretion, and the serum activity of several enzymes--aldolase (ALS), cholinesterase (CHS), leucine aminopeptidase (LAP), isocitrate dehydrogenase (ICD), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBD), creatine kinase (CK), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT)--were estimated in rats with nephrotic syndrome (NS) at 2, 4, 6, 8, 10, 12, 16, 20, and 30 days after a single injection of puromycin aminonucleoside (PAN). It was found that: (a) total serum protein and serum albumin diminished on day 4 and returned to control values on days 20 and 30, respectively; (b) total urine protein excretion rose on day 4, reached a peak value on day 8, and then fell substantially but still remained higher than control values on day 30; (c) ALS and CHS activities increased; (d) LAP, ICD, and AST activities showed a biphasic pattern, first increasing and then decreasing; (e) ALT, LDH, HBD, CK, and ALP activities decreased; and (f) GGT activity remained unchanged. The differences in the profiles of the enzyme activities suggest their independent regulation in experimental NS induced by PAN.

Ischemia-reperfusion induced acute renal failure in the rat is ameliorated by the spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN).

The spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN) reduced the ischemia-reperfusion induced acute renal failure in the rat. Renal ischemia was produced in unilateral nephrectomized rats by complete occlusion of the left renal artery for 60 min. Perfusion of the kidney was then reestablished, and the rats were sacrificed 48 h later.

Urinary excretion of renin and angiotensinogen in nephrotic rats.

Puromycin aminonucleoside (PA)-nephrotic rats have a high plasma renin activity (PRA) and low angiotensinogen levels. We measured proteinuria, urine renin, and urine angiotensinogen daily, for 11 days after PA injection. Proteinuria and urine angiotensinogen were evident on day 5, and urine renin on day 6.

Role of macula densa in diuretics-induced renin release.

Diuretic therapy may enhance renin release by various mechanisms, principally contraction of extracellular fluid volume and its effects, including a fall in arterial pressure. Awake hydropenic or volume-expanded rats received diuretics (amiloride and hydrochlorothiazide) that are known inhibitors of NaCl transport beyond the macula densa; also the well-known Na(+)-K(+)-2 Cl- transport system inhibitor furosemide was administered. We also evaluated the effect of a dose of ethacrynic acid (a drug that shares the same mechanism of action as furosemide but is not diuretic in the rat).

Pathophysiology of experimental nephrotic syndrome induced by puromicyn aminonucleoside in rats. III. Effect of captopril, an angiotensin converting enzyme inhibitor, on proteinuria and sodium retention.

The effect of the converting enzyme inhibitor (CEI) (captopril, 50 mg/kg/day) on proteinuria (UProt), urinary aldosterone (UAldoV), plasma renin activity (PRA), plasma renin concentration (PRC), plasma angiotensinogen concentration (PAC), urinary sodium (UNaV), serum total protein, and body weight was studied for 21 days in an experimental nephrotic syndrome (NS) model induced in rats by a single injection (15 mg/100g) of puromycin aminonucleoside (PA). The effect of captopril on control rats without NS was also characterized. In control rats, captopril increased PRC and PRA, and decreased PAC; it had no effect on UNaV, UAldoV, UProt, total serum protein and body weight.

Serum angiotensin converting enzyme activity and plasma renin activity in experimental models of rats.

1. Serum angiotensin converting enzyme activity (ACEA) and plasma renin activity (PRA) were determined in rats under different experimental conditions such as: nephrotic syndrome (NS), bilateral nephrectomy (BN), renovascular hypertension (RH), dehydration (DEH), anaesthesia (AN), low sodium diet (LSD) and high sodium diet (HSD), and injection with propranolol (PRO) and isoprenaline (ISO). 2.

Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. II. In vitro release of renin, angiotensinogen and aldosterone.

In vitro release of renin, angiotensinogen and aldosterone was studied in control (CT) and nephrotic rats. Nephrotic syndrome (NS) was induced by a single injection of puromycin aminonucleoside (PA). The in vitro systems used were: renal cortical slices (RCS), liver slices (LS) and adrenal glands, all incubated in Krebs-Ringer buffer.

Pathophysiology of experimental nephrotic syndrome induced by puromycin aminonucleoside in rats. I. The role of proteinuria, hypoproteinemia, and renin-angiotensin-aldosterone system on sodium retention.

The pathophysiology of the nephrotic syndrome (NS), characterized by protenuria, edema, sodium retention and hyperlipidemia, is not clear. We studied the role of some systemic factors on sodium retention in an experimental model of NS. NS was induced in rats by a single subcutaneous injection of puromycin aminonucleoside (PA) (15 mg/100 g); control animals received vehicle.

[Intracellular messengers in the regulation of renin secretion].

The intracellular messengers that seem to be involved in renin secretion (RS) from juxtaglomerular cells (JG) are calcium (Ca), cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Unlike the majority of secretory systems, an increase in intracellular Ca concentration and calmodulin and protein kinase C activation inhibit RS. The intracellular Ca concentration in JG cells can be modified if: 1) the normal mechanisms of Ca extrusion of these cells is altered; 2) the calcium output is blocked by lanthanum; 3) the function of the voltage-sensitive Ca-channels is modified; 4) uptake or liberation of Ca from endoplasmic reticulum is modified; 5) plasmatic membrane is bypassed with calcium ionophores such as A 23187.

Evaluating hyperfiltration with glycine in hypertensive rats with renal ablation.

Hypertension-induced renal damage is mediated by increased glomerular pressure and flow. These alterations have been evaluated by the renal response to protein or amino acids. To test this assumption, we studied glomerular hemodynamic responses to glycine infusion in rats with reduced renal mass, with and without Goldblatt hypertension.

Effects of angiotensin-converting enzyme inhibition on altered renal hemodynamics induced by low protein diet in the rat.

We assessed the role of angiotensin II in mediating the alterations in renal hemodynamics known to result from low protein feeding to normal rats by examining the effect of the angiotensin-converting enzyme (ACE) inhibitor captopril. 2 wk of low protein (6% casein) diet resulted in decreased glomerular filtration rate (normal protein [NP], 1.82 +/- 0.

Evaluation of renal functional reserve of contralateral kidney of two-kidney, one clip Goldblatt hypertensive rats.

To evaluate the presence of hyperfiltration in two-kidney, one clip (2K, 1C) Goldblatt hypertensive rats, micropuncture studies of the unclipped kidney were used to examine renal functional reserve (RFR) with glycine (G) infusion in normal (N) rats and 2K, 1C rats. Systemic hypertension in 2K, 1C rats was associated with significantly increased values of single-nephron glomerular filtration rate (SNGFR), glomerular plasma flow (QA) and glomerular capillary hydrostatic pressure (PGC) when compared with N rats. Glycine infusion produced a marked increase in SNGFR, QA and whole-kidney GFR in N rats.

Effect of captopril and hydrochlorothiazide on glomerular haemodynamics and histological damage in Goldblatt hypertension with partial renal ablation.

Increased glomerular capillary pressure (GCP) mediates glomerular damage in hypertension. The efficacy of captopril, an angiotensin converting enzyme (ACE) inhibitor, and captopril-hydrochlorothiazide (captopril-TZ) in lowering GCP and preventing glomerular damage was evaluated in rats with two-kidney, one clip (2K, 1C) Goldblatt hypertension and partial ablation of the unclipped kidney. Thirty days after surgery nine rats received captopril, 11 received captopril-TZ and eight served as untreated control rats.

[A change in glomerular permeability in renovascular hypertension. Participation of angiotensin and structural lesions].

To characterize the decrease in glomerular permeability that occurs in contralateral kidney of renovascular hypertension, glomerular hemodynamics were studied in Goldblatt hypertensive and normotensive control rats. The effects of converting enzyme inhibition (captopril) and renal vasodilatation induced with hyperoncotic plasma were evaluated: in addition, glomerular morphometry was performed. In hypertension, glomerular capillary pressure was increased, ultrafiltration coefficient was decreased, single-nephron filtration rate was normal and afferent resistance was elevated.