PROGESTERONE ADMINISTRATION TO OVARIECTOMIZED RATS REDUCES WATER AND SALT INTAKE INDUCED BY CENTRAL ADMINISTRATION OF ANGIOTENSIN-II

We tested the effects of estradiol, progesterone and testosterone on water and salt intake induced by angiotensin II (ANG II) injected into the third ventricle of female Holtzman rats weighing 250-300 g. The water and salt ingestion observed after 120 min in the control experiments (injection of 0.5 mu l of 0.15 M NaCl into the third ventricle) was 1.6 +/- 0.3 ml (N = 10) and 0.3 +/- 0.1 ml (N = 8) in intact rats, respectively, and 1.4 +/- 0.3 ml (N = 10) and 0.2 +/- 0.1 (N = 8) in ovariectomized rats, respectively. ANG II injected in intact rats (4, 6, 12, 25, and 50 ng, icv, in 0.5 mu l saline) induced an increase in water intake (4.3 +/- 0.6, 5.4 +/- 0.7. 7.8 +/- 0.8, 10.4 +/- 1.2, 11.2 +/- 1.4 ml/120 min, respectively) (N = 43). The same doses of icv ANG II in intact rats increased the 3% NaCl intake (0.9 +/- 0.2; 1.4 +/- 0.3, 2.3 +/- 0.4, 2.2 +/- 0.3. and 2.5 +/- 0.4 ml/120 min, respectively) (N = 42). When administered to ovariectomized rats ANG II induced comparable amounts of water intake (4.0 +/- 0.5, 4.8 +/- 0.6, 6.9 +/- 0.7. 9.6 +/- 0.8, and 10.9 +/- 1.2 ml/120 min, respectively) (N = 43) but there was a significant decrease of 3% NaCl solution ingestion (0.3 +/- 0.1, 0.4 +/- 0.1, 0.8 +/- 0.2, 0.7 +/- 0.2, and 0.6 +/- 0.2 ml/120 min, respectively) (N = 44). Estrogen (50 mu g), progesterone (25 ng), and testosterone (300 mu g) were injected daily into ovariectomized rats for 21 days. Treatment with estrogen decreased the water intake and abolished the saline ingestion induced by icy injection of ANG II (12 ng (2.8 +/- 1.2 and 0.3 +/- 0.1 ml/120 min, respectively) (N = 8). Treatment with progesterone also reduced the water intake (3.3 +/- 0.6 ml/120 min) (N = 8) and abolished the ANG II-induced saline ingestion (0.4 +/- 0.1 ml/120 min) (N = 8), but these effects were not observed with testosterone (6.4 +/- 0.8 and 2.2 +/- 0.3 ml/120 min, respectively) (N = 8). These results indicate that ANG II induces a greater increase in sodium intake in intact female rats than in ovariectomized rats and that estrogen and progesterone impair water and sodium intake in ovariectomized rats.

2-DEOXYGLUCOSE-INDUCED FOOD-INTAKE BY NILE TILAPIA, OREOCHROMIS-NILOTICUS (L)

The alimentary and glycemic responses to cytoglycopenia were studied in thirty-one Nile tilapia alevins of indeterminate sex and age, measuring on average 10.67 +/- 0.82 cm. The cytoglycopenia was provoked by ip injection of 60 mg/kg 2-deoxy-D-glucose (2-DG, N = 16). The control group (N = 15) was submitted to ip injection of 0.2 ml saline. Blood samples for glucose determination were obtained before and three hours after drug administration by cardiac puncture. Food was then offered ad libitum. One hour later the animals were sacrificed and their stomachs removed. The difference in wet weight between full and empty stomach was utilized to quantify the food intake. Median food intake was 0.3877 g for the fish treated with 2-DG and 0.107 g for the animals injected with saline. This difference was statistically significant by the Mann-Whitney test (P<0.05). The median values of blood glucose levels before drug injection were 46.19 mg/100 ml in the 2-DG-treated fish and 44.54 mg/100 ml in the control group. Three hours after drug administration, the values were 48.64 mg/100 ml in the experimental group and 56.90 mg/100 ml in the control group. The difference between the values of blood glucose before and after the drug was not significant for either group. We conclude that glucoprivation provokes food intake in fish and that the same glucoprivation was not sufficient to provoke hyperglycemia.

EFFECT OF LATERAL HYPOTHALAMUS LESIONS ON THE WATER AND SALT INTAKE, AND SODIUM AND URINE EXCRETION INDUCED BY ACTIVATION OF THE MEDIAN PREOPTIC NUCLEUS IN CONSCIOUS RATS

In this-study we investigated the influence of electrolytic lesion of the lateral hypothalamus (LH) on the water and salt appetite, and the natriuretic, diuretic and cardiovascular effects induced by angiotensinergic, cholinergic and noradrenergic stimulation of the median preoptic nucleus (MnPO) in rats. Male Holtzman rats were implanted with a cannula into the MnPO. Other groups of sham- and LH-lesioned rats received a stainless steel cannula implanted into the MnPO. ANGII injection into the MnPO induced water and sodium intake, and natriuretic, diuretic, presser and tachycardic responses. Carbachol induced water intake, and natriuretic, presser and bradycardic responses, whereas noradrenaline increased urine, sodium excretion and blood pressure, and induced bradycardia. In rats submitted to LH-lesion only, water and sodium intake was reduced compared with sham rats. LH lesion also reduced the sodium ingestion induced by ANGII (12 ng) into the MnPO. In LH-lesioned rats, the dipsogenic, diuretic and presser responses induced by ANGII (12 ng), carbachol (2 nmol) and noradrenaline (20 nmol) injection into the MnPO were reduced. The same occurred with sodium excretion when carbachol (2 nmol) and noradrenaline (20 nmol) were injected into the MnPO of LH-lesioned rats, whereas ANGII(12 ng) induced an increase in sodium excretion. These data show that electrolytic lesion of the LH reduces fluid and sodium intake, and presser responses to angiotensinergic, cholinergic and noradrenergic activation of the MnPO. LH involvement with MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested.

Central interaction between atrial natriuretic peptide and angiotensin II in the control of sodium intake and excretion in female rats

We investigated the effects of estrogen on sodium intake and excretion induced by angiotensin II (ANG II), atrial natriuretic peptide (ANP) or ANG II plus ANP injected into the median preoptic nucleus (MnPO). Female Holtzman rats weighing 250-300 g were used. Sodium ingestion and excretion 120 min after the injection of 0.5 mu l of 0.15 M NaCl into the MnPO were 0.3 +/- 0.1 ml (N = 12) and 29 +/- 7 mu Eq in intact rats, 0.5 +/- 0.2 ml (N = 10) and 27 +/- 6 mu Eq in ovariectomized rats, and 0.2 +/- 0.08 (N = 11) and 38 +/- 8 mu Eq in estrogen-treated ovariectomized (50 mu g/day for 21 days) rats, respectively. ANG II (21 mu M) injection in intact, ovariectomized, and estrogen-treated ovariectomized rats increased sodium intake (3.8 +/- 0.4, 1.8 +/- 0.3 and 1.2 +/- 0.2 ml/120 min, respectively) (N = 11) and increased sodium excretion (166 +/- 18, 82 +/- 22 and 86 +/- 12 mu Eq/120 min, respectively) (N = 11). ANP (65 mu M) injection in intact (N = 11), ovariectomized(N = 10)and estrogen-treated ovariectomized (N = 10) rats increased sodium intake (1.4 +/- 0.2, 1.8 +/- 0.3, and 1.7 +/- 0.3 ml/120 min, respectively) and sodium excretion (178 +/- 19, 187 +/- 9, and 232 +/- 29 mu Eq/120 min, respectively). Concomitant injection of ANG II and ANP into the MnPO of intact (N = 12), ovariectomized (N = 10) and estrogentreated ovariectomized (N = 10) rats caused smaller effects than those produced by each peptide given alone: 1.3 +/- 0.2, 0.9 +/- 0.2 and 0.3 +/- 0.1 ml/120 min for sodium intake, respectively, and 86 +/- 9, 58 +/- 7, and 22 +/- 4 mu Eq/120 min for sodium excretion, respectively. Taken together, these results demonstrate that there is an antagonistic interaction of ANP and ANG II on sodium intake and excretion, and that reproductive hormones affect this interaction.

Long-term accumulation of uranium in bones of Wistar rats as a function of intake dosages

Groups of Wistar rats were fed with ration doped with uranyl nitrate at concentration A ranging from 0.5 to 100 ppm, starting after the weaning period and lasting until the postpuberty period when the animals were sacrificed. Uranium in the ashes of bones was determined by neutron activation analysis. It was found that the uranium concentration in the bones. as a function of A, exhibits a change in its slope at similar to20 ppm-a probable consequence of the malfunctioning of kidneys. The uranium transfer coefficient was obtained and an analytical expression was fitted into the data. thus allowing extrapolation down to low doses. Internal and localized doses were calculated. Absorbed doses exceeded the critical dose. even for the lowest uranium dosage.

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Previous studies demonstrated the inhibitory participation of serotonergic ( 5-HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD) in rats. The activity of 5-HT neurons increases after PD- induced 2% NaCl intake and decreases after sodium depletion; however, the activity of the OT neurons appears only after PD-induced 2% NaCl intake. To discriminate whether the differential activations of the 5-HT and OT neurons in this model are a consequence of the sodium satiation process or are the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5-HT- and Fos-OT-immunoreactive neurons in the dorsal raphe nucleus and the paraventricular nucleus of the hypothalamus-supraoptic nucleus, respectively, after isotonic vs. hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD- induced isotonic or hypertonic NaCl intake. Sodium intake induced by PD significantly increased the number of Fos-5- HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and nondepleted animals. The OT plasma levels significantly increased only in the PD- induced 2% NaCl intake group in relation to others, showing a synergic effect of both factors. In summary, 5-HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. In terms of the OT system, both OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals.

Effect of chronic treatment with Clomipramine on food intake, macronutrient selection and body weight gain in rats

Long-term treatment with clomipramine (CMI), a tricyclic antidepressant, induces food craving and body weight gain in patients. The present study investigated the effects of chronic treatment with CMI on total food intake, macronutrient selection, and body weight gain in rats. Male Wistar rats were maintained on a dietary self-selection regime with separate sources of protein, fat and carbohydrate. Animals received i.p. injections of CMI (0, 3, 10, 30 mg/kg) during 27 consecutive days. Food consumption and body weight were recorded daily and results were calculated as average of three consecutive days, namely during pre-treatment (3 d before pharmacological treatment), treatment (7th-9th; l6th-l8th and 25th-27th days), and post-treatment (28th-33rd days). Results showed that CMI (30 mg/kg) significantly decreased energy intake during all treatment period, an effect that was related to a decrease in both carbohydrate-rich diet intake and body weight gain. At dose of 3 mg/kg CMI increased the total energy intake in the 16th-18th days, suggesting an apparent biphasic effect of chronic treatment with CMI on caloric intake. Chronic administration with CMI (27 d) did not alter protein-rich or fat-rich diet consumption. The main result of this study indicated that chronic treatment with CMI decreases rather than increase food consumption and body weight gain in rats exposed to a macronutrient self-selection procedure.

Effect of a non-peptide angiotensin receptor antagonist on water intake caused by centrally administered carbachol in the rat

Angiotensin II (ANG II) administered centrally produces drinking by acting on subtype 1 ANG II (AT1) receptors, Carbachol, a cholinergic receptor agonist, also induces drinking behavior by a central action. In the present study we determined whether the response to carbachol also involves AT1 receptors. Male Holtzman rats (250-300 g) with stainless steel cannula implanted into the lateral ventricle (LV) were used. Water intake after injection of 0.15 M NaCl (1.0 mu l) into the LV was 0.2 +/- 0.01 ml/h (N = 8). The AT1 receptor antagonist DUP-753 (50 nmol/mu l) injected into the LV reduced water intake induced by ANG II (10 nmol/mu l) from 9.2 +/- 1.4 to 0.4 +/- 0.1 ml/h (N = 8), and water intake induced by carbachol (2 nmol/mu l) from 9.8 +/- 1.4 ml/h to 3.7 +/- 0.8 ml/h (N = 8), These results suggest that AT1 receptors play a role in the drinking behavior observed after central cholinergic stimulation in rats.

Antagonism of the renin-angiotensin system and water deprivation-induced NaCl intake in rats

Adult male rats (n = 5-7 per group) were water deprived for 24 h with only food available. Then they had access to water for 2 h. At the end of the 2 h, 1.5% NaCl was offered to the animals and the intake was measured for another 2 h. The rats drank an average of 9.8 +/- 3.0 ml/120 min of 1.5% NaCl; water intake during this time was negligible (not more than 1.0 ml/120 min). Captopril injected IP at the doses of 12 and 24 mg/kg induced 60-90% inhibition of the intake. Losartan or PD123319 injected ICV induced 50-80% inhibition of the intake. Losartan (80 nmol) inhibited the intake at a lower dose than PD123319 (160 nmol). Neither losartan nor PD123319 inhibited 10% sucrose intake. The inhibition of 1.5% NaCl intake was not related to alterations in arterial pressure. The results show that the antagonism of the renin-angiotensin system inhibits the 1.5% NaCl intake induced by water deprivation. The inhibition induced by the angiotensin II antagonists suggest that this peptide is important for the control of salt intake induced by water deprivation.

Isotonic NaCl intake by cell-dehydrated rats

Male adult rats that received an intragastric load of 2 ml of 12% NaCl (n = 13) ingested both water (4.0 +/- 0.2 ml/2 h) and 0.9% NaCl (3.7 +/- 1.0 ml/2 h) when compared with rats that received intragastric load of 2 ml ofwater(water: 0.1 +/- 0.1; 0.9% NaCl: 0.5 +/- 0.3 ml/2 h, n = 12) in a two-bottle test. Intragastric sodium load increased plasma sodium concentration and osmolality by 5% and reduced plasma renin activity by half compared to rats that received intragastric load of water. Intravenous infusion of 1.5 ml/10 min of 10% NaCl (n = 16) also induced ingestion of water (6.2 +/- 0.8 ml/2 h) and 0.9% NaCl (2.9 +/- 0.8 ml/2 h) compared with intravenous infusion of 1.5 ml/10 min of 0.9% NaCl (water: 0.9 +/- 0.4; 0.9% NaCl: 0.5 +/- 0.2 ml/2 h, n = 14). Therefore, a sodium load that raises natremia and plasma osmolality, and therefore induces cell dehydration, results in both 0.9% NaCl and water ingestion when the rats have a two-bottle choice. (C) 2002 Elsevier B.V. All rights reserved.

ROLE OF ADRENERGIC PATHWAYS OF THE MEDIAL PREOPTIC AREA IN ANGII-INDUCED WATER-INTAKE AND RENAL EXCRETION IN RATS

In this study, we investigated the participation of adrenergic neurotransmission in angiotensin II- (ANGII)-induced water intake and urinary electrolyte excretion by means of injection of the alpha(1)-, alpha(2)-, and beta-adrenoceptor antagonists and ANGII into the medial preoptic area (MPOA) in rats. Prazosin (an alpha(1)-adrenergic antagonist) antagonized the water ingestion, Na+, K+ and urine excretion induced by ANGII, whereas yohimbine (an alpha(2)-adrenergic antagonist) enhanced the Na+, K+ and urine excretion induced by ANGII. Propranolol (a nonselective beta-adrenoceptor blocker) antagonized the water ingestion and enhanced the Na+ and urine excretion induced by ANGII. Previous treatment with prazosin reduced the presser responses to ANGII, whereas yohimbine had opposite effects. Previous injection of propranolol produced no effects in the presser responses to ANGII. These results suggest that the adrenergic neurotransmission in the MPOA may actively participate in ANGII-induced dipsogenesis, natriuresis, kaliuresis and diuresis in a process that involves alpha(1)-, alpha(2)-, and beta-adrenoceptors.

Food intake and digestive efficiency in temperate wool and tropic semi-arid hair lambs fed different concentrate: forage ratio diets

This work was conducted to evaluate food intake and digestive efficiency of temperate wool and tropic semi-arid hair lambs, according to different concentrate: forage ratios in diet. Twenty-four lambs, averaging 90 +/- 1.8 days old and a mean body weight of 20 +/- 0.69 kg, 12 of them wool lambs, F, from Ideal x Ile de France crossing, and 12 others pure Santa Ines hair lambs, were distributed into a four replication 3 x 2 factorial arrangement consisting of three diets and two genotypes. Experimental diets consisted of: D1 = 60% concentrate mix (C) and 40% Cynodon sp. cv. Tifton-85 hay (F), D2 = 40% C and 60% F, and D3 = 20% C and 80% F. D1 was formulated for a daily gain of 300g per animal. Increasing forage levels in diets resulted in linear reductions (P < 0.01) in DM, OM, CP, TCH and metabolizable energy (ME) intake, and a linear increase (P < 0.01) in NDF ingestion. Tropic semi-arid hair lambs had higher DM, OM, NDF, CP, and TCH intake than temperate wool lambs. Although there were no genotype effects in OM and GE coefficient of digestibility, hair lambs showed more efficient (P < 0.05) digestibility of DM, CP, NDF and TCH. Increases in forage levels of diets corresponded to a negative linear effect (P < 0.01) in the apparent digestibility of DM, OM, CP, TCH and GE, while apparent digestibility of NDF increased linearly (P < 0.01). Total endogenous nitrogen (fecal plus urinary N) for F(1) Ideal x Ilede France wool and Santa Ines hair lambs were, respectively, 182 and 312 mg/kg(0.75) per day. Thus, Santa Ines tropic semi-arid hair lambs showed to be more responsive than F(1) Ideal x Ile de France temperate wool lambs to low quality fibrous diets. (C) 2004 Elsevier B.V. All rights reserved.

Central moxonidine on water and NaCl intake

In this study we investigated: (a) the effects of intracerebroventricular (i.c.v.) injections of moxonidine (an alpha(2)-adrenergic and imidazoline receptor agonist) on the ingestion of water and NaCl induced by 24 h of water deprivation; (b) the effects of i.c.v. injection of moxonidine on central angiotensin II (ANG II)- and carbachol-induced water intake; (c) the effects of the pre-treatment with i.c.v, idazoxan (an alpha(2)-adrenergic and imidazoline receptor antagonist) and RX 821002 (a selective alpha(2)-adrenergic antagonist) on the antidipsogenic action of central moxonidine. Male Holtzman rats had stainless steel cannulas implanted in the lateral cerebral ventricle. Intracerebroventricular injection of moxonidine (5 and 20 nmol/1 mu l) reduced the ingestion of 1.5% NaCl solution (4.1 +/- 1.1 and 2.9 +/- 2.5 ml/2 h, respectively vs. control = 7.4 +/- 2.1 ml/2 h) and water intake (2.0 +/- 0.6 and 0.3 +/- 0.2 ml/h, respectively vs. control = 13.0 +/- 1.4 ml/h) induced by water deprivation, Intracerebroventricular moxonidine (5 nmol/1 mu l) also reduced i.c.v. ANG Ii-induced water intake (2.8 +/- 0.9 vs. control = 7.9 +/- 1.7 ml/1 h) and i.c.v. moxonidine (10 and 20 nmol/1 mu l) reduced i.c.v. carbachol-induced water intake (4.3 +/- 1.7 and 2.1 +/- 0.9, respectively vs. control = 9.2 +/- 1.0 ml/1 h). The pre-treatment with i.c.v. idazoxan (40 to 320 nmol/1 mu l) abolished the inhibitory effect of i.c.v, moxonidine on carbachol-induced water intake. Intracerebroventricular idazoxan (320 nmol/1 mu l) partially reduced the inhibitory effect of moxonidine on water deprivation-induced water intake and produced only a tendency to reduce the antidipsogenic effect of moxonidine on ANG Ii-induced water intake. RX 821002 (80 and 160 nmol/1 mu l) completely abolished the antidipsogenic action of moxonidine on ANG Ii-induced water intake. The results show that central injections c: moxonidine strongly inhibit water and NaCl ingestion. They also suggest the involvement of central alpha(2)-adrenergic receptors in the antidipsogenic action of moxonidine. (C) 1999 Elsevier B.V.

DECOMPOSITION RATES OF SPENT FUNGAL REFUSE OF ATTA-SEXDENS (HYMENOPTERA, FORMICIDAE) AND IMPLICATIONS FOR ESTIMATING FORAGE INTAKE BY LEAF-CUTTING ANTS

Using simulated ceramic refuse chambers, field decomposition studies were performed on the spent fungal refuse of the lead-cutting ant Atta sexdens rubropilosa. Refuse half life was estimated at 40 days, with complete decomposition at 100 days. These results suggest that the conversion-factor method used to estimate forage input into leaf-cutting ant colonies must be corrected for decomposition, or serious estimation errors will occur.