Cleber G. Gentil

Alterations in sodium chloride and water intake after septal lesions in the rat

Abstract Alterations in sodium chloride and water intake induced by septal lesions employing the standard “two bottle” self-selection procedure were studied. An increase of NaCl and a decrease of water ingestion resulted after placement of the lesions. In rats with bilateral destruction of the septal area changes endured for 2–3 months (end of the experiments) while in those with unilateral lesions the changes subsided after about 45 days. Taking into account previous findings which indicate the role played by the hypothalamus and amygdala in the regulation of NaCl and water intake, it is suggested that impulses come down from the septal area and reach the hypothalamus either directly or indirectly through the amygdala and modulated the activity of hypothalamic regions involved in the regulation of NaCl and water consumption.

Natriuresis, kaliuresis and diuresis in the rat following microinjections of carbachol into 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.

Role of amygdaloid complex in sodium chloride and water intake in the rat.

Abstract Bilateral electrolytic lesions in the amygdaloid complex of the rat elicited either a decrease or increase in 1.5 per cent NaCl intake. The studies were made employing the standard “two bottle” self-selection procedure. Lesions placed in the corticomedial complex, especially the cortical nucleus, resulted in an increase of NaCl and also of the total fluid intake. Bilateral lesions placed principally in the lateral nucleus but also reaching the medial, basolateral and basomedial nuclei resulted in a decrease of NaCl and total fluid ingestion. Sodium balance studies showed that changes in Na consumption preceded changes in urinary output. These results together with those already reported from our laboratory support the assumption of the existence of an intricate circuit related to hydromineral metabolism which involves the septal area, amygdala and hypothalamus.

Lever-pressing behavior caused by intraseptal angiotensin II in water satiated rats.

Abstract Intracerebral injection of angiotensin II induced drinking behavior in satiated rats. In the present experiments five rats, presenting a positve drinking response to the intraseptal injection of angiotensin II, were trained to press a lever for water in a standard chamber, used for operant behavior studies. The injection of 1 μg of angiotensin II into the septal area of the brain caused the animals, previously satiated in the experimental chamber, to resume lever pressing under a continuos reinforcement schedule of water presentation. The number of responses emitted after angiotensin was considerably higher than after a control injection of saline. This result supports the hypothesis that angiotensin has a dipsogenic action in the CNS that mimicks the effect of water deprivation.

Interaction between hypothalamus, amygdala and septal area in the control of sodium chloride intake ☆

Abstract The studies were made in rats employing the standard two-bottle self-selection procedure. Rats with increased salt intake due to lesions in the amygdaloid complex or in septal area diminished their intake following hypothalamic lesions which in the intact rat causes decreases. When the hypothalamic lesions were made first, amygdaloid or septal lesions did not induce any change. Rats with decreased salt intake because of amygdaloid lesions showed an augmented ingestion after septal lesions but if septal lesions were made first the increased intake elicited was not modified by amygdaloid lesions which in the intact rat causes decreases. It was concluded that the hypothalamus is the main structure controlling sodium intake and that the amygdala and septal area have modulating influences on the hypothalamus. In turn, septal area overcomes the action of the amygdala.

Water and sodium chloride intake following microinjections of angiotensin II into the septal area of the rat brain

Abstract The effects of 1 μg of angiotensin II on tap water and 1.5% NaCl intake when injected into the septal area of conscious and unrestrained rats were studied, employing the standard “two bottle” self-selection procedure. Angiotensin yielded a strong dipsogenic action preferentially of tap water. The effect was of short latency and drinking was obsessive. There was not any change in the consumption of food. The drug injected in the dorsal vein of the penis did not shift the intakes of fluids. It was observed in the same group of rats but under nembutal anesthesia that intraseptal angiotensin did not modify the sistemic blood pressure which raised when the drug was given intravenously. The action of angiotensin seems not to be mediated through cholinergic, adrenergic, nor-adrenergic or triptaminergic pathways because neither atropine, propranolol, phentolamine nor methylsergide blocked its dipsogenic effect. Based on some findings the possibility of a direct action of angiotensin on neurons is advanced.

Antagonism of the dipsogenic action of intraseptal angiotensin II in the rat

Abstract The injection of 0.01 to 2.0 μg of antiotensin II (A II) into the medial septal area of unanesthetized rats in normal water balance caused dose-dependent drinking, during the 60 min period following drug administration. A hyperbolic dose-response curve, rectified by a log dose scale was obtained. Pretreatment with 5 and 10 μg of locally injected haloperidol, 15 min prior to A II (0.3 μg), partially antagonized the dipsogenic effects of A II and a dose of 25 μg of haloperidol completely blocked this effect. A cataleptic-like state followed haloperidol administration. The injection of doses as high as 25 μg of dopamine in the same brain site caused no drinking. Pretreatment with 3 μg of intraseptal Sar 1 , Ala 3 , Ile 8 — angiotensin I, a competitive antagonist of A II at peripheral receptors, completely antagonized the dipsogenic effect of A II. The same dose (3 μg) of the A II analog alone caused only a mild but significant drinking response. These results suggest that A II acts of specific receptors in the CNS that may be similar to peripheral angiotensin receptors. On the other hand, the role of brain catecholamines in the mediation of A II-induced drinking remains uncertain.

Taste preferences in a free-choice situation following electrical stimulation and lesion of septal area in rats ☆

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.

Role of adrenals in the changes of sodium chloride intake following lesions in the central nervous system

Abstract To test the neural hypothesis that has been advanced to explain the changes observed in NaCl intake in rats with hypothalamic or amygdaloid lesions the role played by the adrenals in these changes was studied. The experiments were made employing the standard “two bottle” self-selection procedure. Adrenalectomy in rats with increased NaCl ingestion due to hypothalamic or amygdaloid lesions resulted either in no change or decreased intake. Adrenalectomy in rats with diminished consumption following hypothalamic or amygdaloid lesions yielded an increased intake but of lesser intensity than in intact rats. Adrenalectomized rats with corticoid substitutive therapy initiated immediately after the operation to provide normal sodium retaining ability and normal baseline sodium intake when lesioned in the hypothalamus or amygdala showed the same changes as in non-adrenalectomized rats. These results together with others reported in the literature give evidences that NaCl intake can be regulated by extraadrenal factors.

Mechanism of decreased sodium chloride intake after hypothalamic lesions: Effect of hydrochlorothiazide

Abstract In normal rats hydrochlorothiazide has a natriuretic action and in consequence the animal increases salt intake as a homeostatic mechanism. Rats with decreased NaCl ingestion due to hypothalamic lesions failed to show this behavior in spite of the fact that their modifications in urinary and plasmatic sodium were of the same direction as those observed in controls. It seems that the information about sodium concentration and therefore sodium needs is now ineffective because of the interruption of the circuit which normally receives this information. Our results and those published elsewhere support the hypothesis of a neural mechanism underlying the changes observed in rats with decreased NaCl intake due to bilateral anteromedial hypothalamic lesions.