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The thyroid function was studied by means of a comparison between rats that drank daily less than 2 mEq of a NaCl solution (control) and rats that spontaneously drank daily above 4 mEq of this solution (0.25 M), which is considered aversive to rats. It was found that, in these rats, the protein-bound iodine (PBI-127) and the radioactive iodine uptake (I-131) were less than in the control rats, in spite of similar thyroid weight. It seems, therefore, that the rats that drank high levels of the aversive salt solution have hypothyroidism. This finding shows another link between the thyroid gland and NaCl intake. These data have implications in the design and interpretation of experiments in which NaCl intake is studied.

1. The present study was undertaken to investigate the influence of the septal area on neural mechanisms involved in feeding behavior elicited by electrical stimulation of the lateral hypothalamic area of the rat. 2. Electrolytic damage to medial and lateral septal nuclei induced a significant increase (18.29 +/- 1.69 to 25.05 +/- 2.31 g, P less than 0.05, N = 14) in food intake elicited by hypothalamic stimulation. The threshold current for stimulus-induced eating decreased by 20% after septal lesion. 3. A significant decrease in food ingestion was observed after electrical stimulation of the septal nuclei, either preceding (27.47 +/- 1.57 to 19.30 +/- 2.06 g, P less than 0.05, N = 13) or simultaneous (26.20 +/- 1.60 to 12.10 +/- 2.40 g, P less than 0.05, N = 11) with hypothalamic stimulation. 4. The results indicate an inhibitory effect of the septum on the lateral hypothalamic area and also suggest that the functional state of the lateral hypothalamus, which is responsible for the feeding behavior, depends on the activity pattern of the septal area.

In the present study, electrical stimulation of medical or laternal septal areas and total or restricted lesions of these were conducted to observe the effect on ingestion of primary taste solutions in a free-choice situation. Stimulation induced a specific decrease in the intake of NaCl solution and had no effect on saccharin, acetic acid and quinine solutions and water. Total septal lesion or restricted lesions of medial or lateral septal areas induced hyperdipsia in rats. The lesioned rats, in a free-choice situation preferred NaCl, saccharin, as well as acetic acid solutions. This increase in acetic acid intake after lesion suggests that sour taste is also affected. Furthermore, there was no consumption of quinine solution before and after the lesion. This might be due to the presence of sweet tasting saccharin solution in this free-choice situation. These results indicate that the septal area causes aversion to NaCl intake, probably by inhibiting lateral hypothalamic neurons responsible for NaCl ingestion. The consumption of large quantities of saccharin, NaCl and acetic acid after the septal lesion suggests that the rats become overresponsive to taste factors in a free-choice situation.

Luteinizing hormone (LH) secretion by the anterior pituitary gland was investigated in hemidecorticate (HD) rats under several conditions. Higher plasma and lower pituitary LH levels were observed in HD rats in the afternoon of proestrus, after unilateral ovariectomy, and at the 7th and 14th days after bilateral castration. The ovarian hypertrophy observed in HD rats did not differ from control. When hormonal substitutive therapy was started 3 days after bilateral ovariectomy, larger doses of estradiol benzoate (EB) were required to reduce plasma LH levels in control than in HD animals. The increase in pituitary weight was, however, significantly higher in the HD castrated group. When substitutive therapy started at the 7th and 14th days after castration no significant differences between the 2 experimental groups were observed. The results of substitutive therapy suggest that hemidecortication induces an increase in the sensitivity of hypothalamic-pituitary axis to estrogen negative feedback. This change in sensitivity is clearly seen in HD rats during the first few days after castration. These results suggest that hemidecortication may release the hypothalamus from inhibitory influences coming from rhinencephalic or cortical structures, thus rendering the preoptic-suprachiasmatic complex (POA-SCH) more sensitive to LH-releasing mechanisms.

The effects of adrenergic stimulation of the lateral hypothalamic area on sodium and potassium excretion were studied in rats bearing implanted cannulae. When noradrenaline was injected into several points of the lateral hypothalamic area, a dose-related increase in natriuresis and kaliuresis was observed. Rats previously injected through the same cannulae with alpha (Regitine) or beta (Propranolol) blocking agents showed different natriuretic responses when injected with noradrenaline. It was observed that the normal noradrenaline-induced natriuresis was abolished by the alpha-adrenergic blockers, while beta-adrenergic blockers increased the response. Intrahypothalamic injection of Isoproterenol, and activator of the beta-adrenergic receptor, induced a decrease in natriuresis, kaliuresis and urinary volume. In contrast, injection of Metaraminol, an alpha-adrenergic agonist, caused an increase in sodium and potassium excretion and a reduction of urinary volume. Drugs blocking the destruction of noradrenaline or its reuptake by the presynaptic nerve endings potentiated 2-fold the action of 20 nmol of noradrenaline. These experiments provide good evidence for the existence of an adrenergic mechanism consisting of alpha and beta receptors which works antagonistically on the regulation of sodium and potassium excretion. The excretion on the two electrolytes is stimulated by the alpha-adrenergic system, and inhibited by the beta-adrenergic system.

Urinary output of Na+ and K+, and volume of urine have been studied in conscious, unrestrained, water-loaded male rats following the intraseptal injection of catecholamines. Natriuresis and kaliuresis increased after injecting noradrenaline (NA), the intensity being dose related. The dose-response curve suggests that a monomolecular interacting takes place between NA and pharmacological receptors present in the septal area. No change was observed in diuresis. Systematic mapping of the septal area yielded about the same results for all sites except a zone located in the lateral nucleus that was more sensitive. An alpha blocker (dibenamine), injected intraseptally before NA, showed an inhibitory effect while a beta blocker (propranolol) yielded a potentiation effect. These same effects of the blocking agents were observed when adrenaline was used instead of NA. Lidocaine, which inhibits the re-uptake of NA, showed an enhancement of the natriuretic and kaliuretic effect of NA, and the same effect was observed when the enzymatic destruction of NA was prevented by nialamide, an inhibitor of monoaminoxidase. Dopamine showed a natriuretic effect, but no effect was observed on K+ and urine output. Serotonin had no action on natriuresis, kaliuresis and diuresis.

The effect of intraseptal injection of carbachol and nicotine on urinary output of Na+ and K+ in untreated rats as well as in animals pretreated with locally injected atropine, hexamethonium, dibenamine and propranolol was studied in order to evaluate the relative role played by central muscarinic and nicotinic receptors in the regulation of salt and water renal excretion. The injection of 30-250 nmol of nicotine into the medial septal area caused a dose-dependent increase in Na+ and K+ urinary output whereas urine volume was little affected. The effect of 30 nmol of nicotine was blocked by pretreatment with 100 nmol of hexamethonium. In addition, pretreatment with 5 nmol of either hexamethonium or atropine partially antagonized the natriuretic and kaliuretic effect of 1 nmol of carbachol. Also the alpha-blocking agent, dibenamine (150 nmol) antagonized, while the beta-blocker, propranolol (100 nmol) significantly enhanced the effect of carbachol. Propranolol (100 nmol) alone caused a small, but significant increase in Na+ and K+ renal excretion. These results indicate that stimulation of both muscarinic and nicotinic receptors in the septal area, as caused by carbachol, elicits increased disposition of Na+ and K+ by the kidneys. Also, part of the effects of carbachol appear to be mediated by the release of endogenous catecholamines, acting on central alpha receptors to increase Na+ and K+ urinary excretion. On the other hand, simultaneous activation of beta-receptors by the released amines would partially inhibit this effect.

Bipolar stainless steel electrodes or stainless steel cannulas were implanted stereotaxically into the lateral hypothalamus of rats. Drinking was elicited by electrical or chemical (carbachol or angiotensin II) stimulation of animals, which were offered water and solutions of sodium chloride, saccharin, acetic acid and quinine. During electrical stimulation, ingestion of water and of all the solutions increased significantly. The same rats ingested significantly more sodium chloride and saccharin solution after 23 h water deprivation and electrical stimulation of the lateral hypothalamus. Carbachol administered into the lateral hypothalamus induced ingestion of saccharin solution and water but not of sodium chloride. Angiotensin II injected into the lateral hypothalamus did not induce drinking in most of the rats and those which drank preferred sodium chloride, saccharin and water. Several of the rats which did not respond to angiotensin II injection into the lateral hypothalamus, 72 h after angiotensin II responded to injection of carbachol by drinking the saccharin solution. The results of electrical stimulation suggest that the lateral hypothalamus consists of neurons involved in the ingestion of primary taste solutions. Depending on the functional state of the organism, lateral hypothalamic stimulation modifies ingestion of other taste substances but not of salt, as indicated by water deprivation. Chemical stimulation indicates that the neurotransmitter responsible for salt intake is not cholinergic and that the cholinergic neurons evoke preference for sweet taste and water. It appears that angiotensin II is involved in salt intake, as well as in producing preference for sweet taste and water.

To study the role played by neurotransmitters and their receptor mechanisms in the control of feeding behavior elicited by electrical stimulation, drugs that affect neurotransmission were injected via cannula electrodes into the lateral hypothalamic area. Pretreatment with noradrenaline (0.5 and 1.0 nmol) significantly increased the effect of hypothalamic stimulation on feeding, whereas injection of 1.0, 2.0 and 4.0 nmol of adrenaline or dopamine was ineffective. Phentolamine (40.0, 80.0 and 100.0 nmol) and propranolol (40.0, 80.0 and 120.0 nmol) induced a decrease in food intake, suggesting the involvement of both alpha and beta receptors in this mechanism. However, isoprenaline (20.0 nmol) also reduced food intake. Reduction of food intake by propranolol was probably related to the action of the local anesthetic. Alphamethyl-p-tyrosine (203.0 nmol), reserpine (32.8 nmol) and 6-hydroxydopamine (200.0 nmol) inhibited the feeding behavior elicited by electrical stimulation of the lateral hypothalamic area. These results suggest that electrical stimulation of the lateral hypothalamic area elicits feeding behavior by releasing noradrenaline. Alpha-adrenergic receptors seem to play a facilitatory role in feeding behavior.

Cholinergic and adrenergic agonists and antagonists were injected directly into the subfornical organ (SFO), via implanted cannulae, and the volume of water ingested was recorded over a period of 1 hour after injection. Application of 2 nmol carbachol caused intense water intake in 100% of the animals (8.78 +/- 0.61 ml), with a very short intake latency. When the 2 nmol carbachol dose was preceded by increased doses of atropine, a progressive reduction in water intake was observed, with complete blockage of the thirst-inducing response to carbachol at the 20 nmol dose level with atropine. Followed by several doses of hexamethonium, the water intake caused by application of 2 nmol carbachol was reduced, although the response was not totally blocked. Injection of 80 nmol of nicotine had a significant thirst-inducing effect in 50% of the animals studied (1.06 +/- 0.18 ml) and increase in water intake was further reduced by application of increased doses of hexamethonium. Raising the dose levels of noradrenaline into the SFO caused an increase in water intake although to a lesser degree than was observed after carbachol injection. When the 40 nmol dose of noradrenaline was preceded by increased doses of propranolol (5 to 40 nmol), there was a gradual reduction in water intake, with total blockage at the 40 nmol dose. Application of phentolamine in doses of 10 to 80 nmol caused no reduction in water intake after 40 nmol of noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Rats bearing lesions in the septal area (SA), or in the subfornical organ (SFO) or simultaneously in both regions were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesion of the SA drank more water than either normal rats or SFO-lesioned animals under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by SA lesions was blocked after SFO lesions. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in SFO-lesioned animals even after destruction of the SA. Animals with SFO lesions did not show increase of the water intake after cellular dehydration. The results obtained suggest that the SFO acts as the main structure in the regulation of water intake elicited by angiotensin with two opposite effects: one direct, facilitating water intake and the other indirect inhibiting the SA. The SA has an inhibitory effect on the SFO and on water intake.

The present study examined the effects of carbachol and angiotensin II injected into the medial and lateral septal areas (MSA and LSA) on the ingestion of primary taste solutions in a free-choice situation. The injection of carbachol or angiotensin II into MSA and LSA of water sated rats evoked a preference for the sweet tasting saccharin solution and water. The lateral septal rats also preferred acetic acid solution. Only the total fluid intake differed significantly among the four groups. In the water deprived rats injection of chemical to the respective groups induced the ingestion of NaCl solution. The MSA rats on injection of carbachol also preferred saccharin apart from NaCl. There was a significant difference in the NaCl intake among the four groups. The quinine solution was not consumed by all the groups. These results indicate that both the carbachol and angiotensin II induce the ingestion of saccharin, NaCl and water. The MSA might be more sensitive in inducing NaCl intake as compared with LSA during deprivation schedule and cholinergic stimulation. The LSA also evokes a preference for the sour tasting acetic acid. Furthermore, the data also suggest that the neurons sensitive to angiotensin are more potent than cholinergic neurons of LSA in producing salt preference.

By using the two-bottle, self-selection method it was found that an excess of thyroid hormone administration to rats increased water and sodium intake. Thyroidectomy changed the initial preference from water to sodium chloride. Oral treatment of the thyroidectomized rats with thyroid hormones brought salt ingestion back to normal levels and greatly augmented the water intake. Two-week treatment was followed by an increase in salt intake, which was characterized by large oscillations resembling the corresponding effects of adrenalectomy and treatment with deoxycorticosterone.

Since lesion of subcortical structures may affect the barbiturate sleeping time (bST), we decided with the present study to elucidate the role of the caudate nucleus in the determination of central sensitivity to barbiturates. Rats implanted with a cannula in the caudate nucleus of one or both sides, as well as with a jugular cannula, were utilized. Intravenous injections of sodium pentobarbital (40 mg/kg), intracerebral injections of Xylocaine (0.04 microgram), carbachol (0.2 micrograms) or artificial cerebrospinal fluid (ACF) into the caudate nucleus were performed. Both Xylocaine and carbachol, but not ACF, increased the bST regardless of the preparation used, the only exception being Xylocaine which did not alter the bST, if injected into the left caudate nucleus. The results suggest that the caudate nucleus may act as a modulator of the central sensitivity to barbiturates.

In this study, the participation of the adenylcyclase--cAMP system of the rat septal area in the mediation of the natriuretic, kaliuretic and diuretic effects of noradrenaline (NA) was investigated. The intraseptal injection of 20 nmol of NA caused a significant increase in the urinary excretion of Na+ and K+ as well as in the urinary volume during the 2 hr period following the intracerebral injection which was blocked by 40 nmol of phentolamine, locally injected, 30 min before the catecholamine. In contrast, pretreatment with propranolol (100 nmol) potentiated the effects of NA on salt and water renal excretion. The intraseptal injection of 3.12 to 50 nmol of dibutryrl cyclic adenosine monophosphate (db cAMP) caused dose-dependent increase in natriuresis and kaliuresis, but a decrease in urinary volume. Under the same experimental conditions, caffeine administration (6.25 to 100 nmol) also induced dose-dependent increases in Na+ and K+ urinary output. These results indicate that the saluretic effect of NA may be mediated by an alpha receptor-induced activation of the adenylcyclase--cAMP system in the septal area.

The effects of intraseptal injection of carbachol on natriuresis, kaliuresis and diuresis has been studied in conscious, unrestrained water-loaded male rats. Urinary sodium and potassium excretion increased following injections into the septal area. The intensity of the natriuresis and kaliuresis was dose-related. An antidiuretic effect was also observed. The Na+/K/ ratio increased with increasing doses of carbachol, indicating that the rise in urinary sodium exceeded that of potassium. Systematic mapping of the septal area yielded about the same results for all sites, excepting a zone located in the anterior-dorsal part of the medial nucleus which appeared more sensitive. The natriuretic effect of intraseptal carbachol in adrenalectomized rats demonstrated the secondary role played by the adrenals. Contrariwise the decrease of the natriuretic effect observed either in hypophysectomized rats or in rats bearing a median eminence lesion receiving intraseptal carbachol showed the important participation of these structures in urinary Na+ excretion. Adrenalectomy or median eminence lesions did not modify the kaliuretic response while hypophysectomy produced a transitory diminution. This fact favours the hypothesis of different mechanisms involved in Na+ and K+ excretion following intraseptal carbachol. These results leave open the question as to mechanism of action but suggest a possible role of the pituitary in mediating the responses. Also, the possibility of a role played by hemodynamic shifts is suggested.

Sodium chloride intake was studied in rats submitted to different neurosurgical procedures. Intake decreased in animals submitted to bilateral destruction of the basolateral amygdaloid complex, and increased after the same animals were submitted to destruction of the anterior lateral hypothalamus, a procedure which is known to cause increased intake in intact rats. In the reverse experiment, where the anterior lateral hypothalamus was destroyed before the basolateral amygdaloid complex, the effect of increased sodium chloride intake induced by destruction of the hypothalamus overcame the decreased expected upon destruction of the amygdaloid complex. These results permit us to conclude that the hypothalamic areas which inhibit sodium chloride intake predominate over the stimulating areas of the amygdaloid complex in the control of sodium chloride intake.