Bombesin affects the central nervous system to produce sodium intake inhibition in rats

Bombesin (BN) elicits in the rat important behavioural modifications, including inhibition of food and of water intake. Recently, it has been observed that the peptide also inhibits the intake of sodium chloride. To stare whether BN possesses a selective antinatriorexic effect or it elicits only an aspecific depression of ingestive behaviour, we studied the effects of this peptide on the intake of sodium, water or sucrose of Wistar rats after injections into the fourth brain ventricle or into selected brain areas involved in the control of sodium intake, containing BN-like peptides and/or their precursors or specific receptors. We observed that: a) BN (100-200 ng/rat) injected into the fourth brain ventricle inhibits not only the intake of 2% NaCl of sodium depleted rats but also that of water and of 5% sucrose; b) BN (5-50 ng/rat) administered into the nucleus of the solitary tract and the medial amygdala does not influence the intake of these fluids and c) BN (5-50 ng/rat) injected into the paraventricular nucleus does not influence the intake of water and 5% sucrose but potently inhibits that of 2% NaCl. We concluded that the inhibitory effect elicited on salt intake by intracranial administration of BN is selective for this behaviour and is not the expression of an aspecific depression of ingestive behaviour. (C) 1998 Elsevier B.V.

Effects of subtypes alpha- and beta-adrenoceptors of the lateral hypothalamus on the water and sodium intake induced by angiotensin II injected into the subfornical organ

The present experiments were conducted to investigate the role of the alpha (1A)-, alpha (1B), beta (1),- and beta (2)-adrenoceptors of the lateral hypothalamus (LH) on the water and salt intake responses elicited by subfornical organ (SFO) injection of angiotensin II (ANG II) in rats. 5-methylurapidil (an alpha (1A)-adrenergic antagonist), cyclazosin (an alpha (1B)-adrenergic antagonist) and ICI-118,551 (a beta (2)-adrenergic antagonist) injected into the LH produced a dose-dependent reduction, whereas efaroxan (an alpha (2)-antagonist) increased the water intake induced by administration of ANG II into the SFO. These data show that injection of 5-methylurapidil into the LH prior to ANG II into the SFO increased the water and sodium intake induced by the injection of ANG II. The present data also show that atenolol (a beta (1)-adrenergic antagonist), ICI-118,551, cyclazosin, or efaroxan injected into the LH reduced in a dose-dependent manner the water and sodium intake to angiotensinergic activation of SFO. Thus, the alpha (1)- and beta -adrenoceptors of the LH are possibly involved with central mechanisms dependent on ANG II and SFO that control water and sodium intake. (C) 2000 Elsevier B.V. B.V. All rights reserved.

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.

Potassium intake during cell dehydration

Isotonic NaCl is ingested in addition to water by cell-dehydrated rats in two-bottle tests. The objective of the present work was to find out whether mineral intake in the cell-dehydrated rat is specific to NaCl in a five-bottle test. Adult male Sprague Dawley rats had distilled water and four mineral solutions at palatable concentrations (0.01 M KCl, 0.05 mM CaCl2, 0.15 M NaHCO3, 0.15 M NaCl) simultaneously available for consumption. Cell-debydration was produced infusing 1.5 ml of NaCl solution (0.15, 0.25, 0.5, 1.01, 2.0, 4.0 M) intravenously for 10 min and intakes were recorded for the next hour. It was observed a NaCl concentration-dependent increase in 0.01 M KCl intake. The ingestion of the other mineral solutions was not significantly altered compared to infusion of 0.15 M NaCl. The ingestion of KCl was not related to changes in serum potassium concentration. The ingestion of KCl was reduced in half and water was the preferred fluid when the five-bottle test was performed with mineral solutions at isomolar (0.15 M) concentrations. There was no increase in intake of other mineral solution in the isomolar test. No preference was observed for palatable or isomolar solutions during early extracellular dehydration until 4 h after subcutaneous injection of furosemide, in spite of the increase in total volume intake. Therefore, mineral intake induced by cell dehydration is not specific for NaCl solution. The type of mineral solution available influences the choice and KCl. is the preferred solution of the cell-dehydrated rat in the conditions of the present study. (c) 2005 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.

Estimativas do Consumo e da Taxa de Passagem do Capim-Elefante (Pennisetum purpureum Schum.) sob Pastejo de Vacas em Lactação

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

Angiogenesis, under normal conditions, is a tightly regulated balance between pro- and antiangiogenic factors. The goal of this study was to investigate the mechanisms involved in the control of the skeletal muscle angiogenic response induced by electrical stimulation during the suppression of plasma renin activity (PRA) with a high-salt diet. Rats fed 0.4% or 4% salt diets were exposed to electrical stimulation for 7 days. The tibialis anterior ( TA) muscles from stimulated and unstimulated hindlimbs were removed and prepared for gene expression analysis, CD31-terminal deoxynucleotide transferase-mediated dUTP nick-end labeling ( TUNEL) double-staining assay, and Bcl-2 and Bax protein expression by Western blot. Rats fed a low-salt diet showed a dramatic angiogenesis response in the stimulated limb compared with the unstimulated limb. This angiogenesis response was significantly attenuated when rats were placed on a high-salt diet. Microarray analysis showed that in the stimulated limb of rats fed a low-salt diet many genes related to angiogenesis were upregulated. In contrast, in rats fed a high-salt diet most of the genes upregulated in the stimulated limb function in apoptosis and cell cycle arrest. Endothelial cell apoptosis, as analyzed by CD31-TUNEL staining, increased by fourfold in the stimulated limb compared with the unstimulated limb. There was also a 48% decrease in the Bcl-2-to-Bax ratio in stimulated compared with unstimulated limbs of rats fed a high-salt diet, confirming severe apoptosis. This study suggests that the increase in endothelial cell apoptosis in TA muscle might contribute to the attenuation of angiogenesis response observed in rats fed a high-salt diet.

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.

EFFECT OF CHOLINERGIC STIMULATION OF THE AMYGDALOID COMPLEX ON WATER AND SALT INTAKE

The effect of carbachol (80 nmol/mul) injection into the amygdaloid nuclear complex (AMG) on sodium appetite and water intake was studied in male Holtzman rats weighing 240-270 g. Twenty-five satiated rats and 38 water-deprived rats were used in the experiment on water intake. In the experiment on sodium intake, 19 rats were injected with atropine + carbachol and 9 rats with hexamethonium + carbachol. After carbachol injection into the AMG, water intake decreased in rats submitted to 30 h of water deprivation (10.28 +/- 1.04 ml/120 min vs 0.69 +/- 0.22 ml/120 min). The decrease in water intake was blocked by prior local injection of a tropine (20 nmol/1 mul)(11.66 +/- 1.46 ml/120 min vs 0.69 +/- 0.22 ml/120 min), but not of hexamethonium (30 nmol/1 mul), into the AMG. In water-deprived animals, carbachol injection into the AMG caused a decrease in sodium chloride intake (6.16 +/- 1.82 ml/h vs 0.88 +/- 0.54 ml/h) which was blocked by previous injection of hexamethonium but not of a tropine. These results suggest that the cholinergic system of the AMG plays a role in the control of water and salt intake.