High blood pressure is one of the symptoms of paraquat-induced toxicity in rats.

This study investigated whether paraquat (Pq)-induced lipidic peroxidation (LP) is accompanied by changes in blood pressure and heart rate (HR) in rats. Groups of adult male Wistar rats were studied 2 and 12 h after Pq (35 mg/kg, i.p.) administration. The LP was evaluated by monitoring thiobarbituric acid reactive substances (TBARS) in the kidneys, liver and lungs, and validated by including a group treated with an antioxidant, superoxide dismutase (CuZnSOD 50,000 IU/kg), in the study. The TBARS levels were significantly higher (p<0.05) in the kidneys of the rats studied 2 h after Pq than in their respective controls. Similarly, systolic and diastolic blood pressure (DBP) were higher (p<0.05), while HR was lower (p<0.05) than basal levels 2 and 12 h after Pq administration. In contrast, the group treated simultaneously with Pq and CuZnSOD exhibited lower levels of TBARS (p<0.05) in all studied organs compared to the control group, while the mean arterial pressure and HR did not differ from those seen in the control group. These findings indicate that acute Pq poisoning symptoms include high blood pressure.

Regional Brazilian diet-induced low birth weight is correlated with changes in renal hemodynamics and glomerular morphometry in adult age.

Number of nephrons, renal hemodynamics, and glomerular morphometry were assessed in rats submitted to a multideficient diet which was developed from a basic regional diet consumed in a Brazilian region of sugarcane cultivation. We evaluated three groups of male Wistar rat offspring: (1) from dams fed a standard diet throughout mating, pregnancy and lactation (control group) and (2) from dams fed the multideficient diet during mating and pregnancy (MalN1 group) or (3) throughout mating, pregnancy, and lactation (MalN2 group). At adult age, the animals were anesthetized to measure mean arterial blood pressure and renal hemodynamics. The MalN1 group, as compared with the control group, showed unaltered body and kidney weights, nephron deficiency, a high mean arterial blood pressure, glomerular hypertrophy, and renal vasoconstriction. The MalN2 group showed the same nephron deficiency and mean arterial blood pressure levels as the MalN1 group. These animals exhibited lower body and kidney weights and no glomerular hypertrophy. In conclusion, the alterations induced by intrauterine malnutrition are compatible with the development of chronic renal failure.

Renal hemodynamic response to erythropoietin-induced polycythemia in 5/6 nephrectomised rats is different from normal rats.

The effects of recombinant human erythropoietin (rHuEPO)-induced polycythemia on renal function and glomerular hemodynamics were evaluated in Munich-Wistar rats (MW+EPO) before and after infusion of indomethacin; the rHuEPO effects on total renal function were also evaluated in 5/6 nephrectomized (CRF) MW and spontaneously hypertensive rats (MW-CRF+EPO and SHR-CRF+EPO, respectively). In normal MW rats, rHuEPO (300 IU/kg BW, 3 x /week, during 2 weeks) induced elevation in MAP, with maintenance of GFR, paralleled by superficial vasodilatation and elevation in SNGFR, suggesting cortical blood redistribution. These hemodynamic alterations induced by rHuEPO were blunted by indomethacin, suggesting a participation of the vasodilator prostaglandins in the renal compensatory mechanism of polycythemia. Elevation in MAP and reduction in GFR occurred in the MW-CRF+EPO group compared with the group receiving vehicle. In contrast, the SHR-CRF+EPO presented a reduction in MAP and maintenance of GFR, suggesting different rHuEPO effects depending on previous renal function and/or hypertensive state.

Diuretic, natriuretic and kaliuretic effects of dexamethasone.

We report the diuretic, natriuretic and kaliuretic effects of dexamethasone (DEXA) on intact and adrenalectomized (ADX) male Wistar rats. Indomethacin (INDO) and spironolactone were used to evaluate the involvement of prostaglandin and mineralocorticoid receptors in these actions. DEXA (400 micrograms/kg) and INDO (20 mg/kg) were injected iv and spironolactone (8 mg/100 g) was administered by the oral route. The parameters analyzed were urinary volume (UV), sodium excretion (UNaV) and potassium excretion (UKV). DEXA increased UV and UKV in both intact and ADX rats. INDO administered to intact rats reduced UV by 28% (P less than 0.05) and caused anuresis in ADX rats, but did not interfere with the increased UV induced by DEXA in either ADX or intact animals. Spironolactone did not interfere with diuretic parameters in control animals, but in DEXA-treated animals it decreased UKV by 30% and inhibited DEXA-induced diuresis. These data rule out the possibility of prostaglandin involvement in the acute effects of DEXA and suggest that DEXA induces diuresis through its action on mineralocorticoid receptors or on specific receptors for glucocorticoid (the type II receptor). The latter might also be inhibited by spironolactone.

Diuretic, natriuretic and kaliuretic effects of dexamethasone

1. Thrombus formation induced by electrical stimulation of the carotid artery was investigated in anesthetized rabbits and rats. Occlusive Grade III thrombi were produced consistently in 34 normal New Zealand rabbits and 58 untreated albino Wistar rats. Thrombus formation was monitored continuously in some of the animals with a magnetic flowmeter or a thermistor probe applied on the carotid. 2. The usefulness of the model for the screening of drugs was tested by treating the animals with warfarin, heparin, prostacyclin (PGI2), dihydroprostacyclin (DiHPGI2), prostaglendin E1 (PGE1), and prostaglandin D2(PGD2). 3. All of the drugs except warfarin were infused continuously into the venous circulation during the entire experimental period at a rat of 0.2 ml/min. 4. Warfarin (10 mg/Kg), administered by gavage 24 h before experimental, prevented thrombus formation, as did heparin iv (> 34 U/Kg). 5. Of the four platelet antiaggregatory prostaglandins tested, PGI2 was the most potent inhibitor of thrombus formation and DiHPGI2 the least active, as evaluated by visual inspection of stimulated arterial segments which were excised 30 min (rabbits) or 15 min (rats) after the stimulation was stopped. PGI2 was less active in rats than in rabbits (Threshold Protective Dose ratio ca. 4:1). PGE1 and PGD2 showed intermediate activity in both animal models