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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.

Rats bearing lesions in the septal area followed by lesions in the subfornical organ were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesions of the septal area drank more water than either during the control period or after lesion of the subfornical organ under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by lesions in the septal area was blocked after lesion of the subfornical organ. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in animals whose subfornical organ had been destroyed. Animals with lesions in the subfornical organ showed decreased water intake after cellular dehydration. The results obtained suggest that the subfornical organ acts as a more important structure than the septal area in the regulation of water intake elicited by angiotensin, with two opposite effects: a direct one facilitating water intake, and an indirect one inhibiting the septal area. The septal area has an inhibitory effect on the subfornical organ and on water intake.

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.