Effects of the alpha antagonists and agonists injected into the lateral hypothalamus on the water and sodium intake induced by angiotensin II injection into the subfornical organ.

The subfornical organ (SFO) and the lateral hypothalamus (LH) have been shown to be important for the central action of angiotensin II (ANG II) on water and salt regulation. Several anatomical findings have demonstrated neural connections between the SFO and the LH. The present experiments were conducted to investigate the role of the alpha-adrenergic antagonists and agonists injected into the LH on the water and salt intake elicited by injections of ANG II into the SFO. Prazosin (an alpha1-adrenergic antagonist) injected into the LH increased the salt ingestion, whereas yohimbine (an alpha2-adrenergic antagonist) and propranolol (a beta-adrenergic antagonist) antagonized the salt ingestion induced by administration of ANG II into the SFO. Previous administration of clonidine (an alpha2-adrenergic agonist) or noradrenaline into the LH increased, whereas pretreatment with phenylephrine decreased the sodium intake induced by injection of ANG II into the SFO. Previous treatment with prazosin and propranolol reduced the water intake induced by ANG II. Phenylephrine increased the dipsogenic responses produced by ANG II, whereas previous treatment with clonidine injected into the LH reduced the water intake induced by ANG II administration into the SFO. The LH involvement with SFO on the excitatory and inhibitory mechanisms related to water and sodium intake is suggested.

Reduction of liver mass due to malnutrition in rats. Correlation with emaciation of animals and size of organs not inserted in the portal system.

We studied the effects of protein-energy malnutrition on the liver morphology of rats as compared to animal emaciation and to reduction in size of the organs not irrigated by splanchnic blood such as kidneys and spleen. The animals were divided into two groups, one of them fed ad libitum rate (N = 10) and the other (N = 14) receiving water but no food for 7 days, and the changes in animal weight, liver, kidney and spleen mass were determined. DNA and the protein/DNA ratio, as well as hepatocyte size, were determined in liver tissue. The liver decreased in mass (27.14%) at a significantly higher proportion (p < 0.05) when compared to body emaciation (19.22%). Similar to the reduction in body weight, the masses of kidneys and spleen were reduced by 18.68% and 24.28%, respectively. The reduction in liver mass occurred due to hypoplasia and atrophy, i.e., a decrease in hepatocyte number and size, respectively. We conclude that there is a preferential consumption of liver protein in protein-energy malnutrition which is suggested to result from the additive action of the effects of overall consumption of organic reserves due to malnutrition proper and to the reduction of the hepatotrophic stimulus.

Alpha-adrenergic pathways in the lateral hypothalamus are important for the dipsogenic effect of carbachol injected into the medial septal area.

We studied the effect of the alpha 1- and alpha 2-adrenergic receptors of the lateral hypothalamus (LH) on the control of water intake induced by injection of carbachol into the medial septal area (MSA) of adult male Holtzman rats (250-300 g) implanted with chronic stainless steel cannulae into the LH and MSA. The volume of injection was always 1 microliter and was injected over a period of 30-60 s. For control, 0.15 M NaCl was used. Clonidine (20 nmol) but not phenylephrine (160 nmol) injected into the LH inhibited water intake induced by injection of carbachol (2 nmol) into the MSA, from 5.4 +/- 1.2 ml/h to 0.3 +/- 0.1 and 3.0 +/- 0.9 ml/h, respectively (N = 26). When we injected yohimbine (80 nmol) + clonidine (20 nmol) and prazosin (40 nmol) + clonidine (20 nmol) into the LH, water intake induced by injection of carbachol into the MSA was inhibited from 5.4 +/- 1.2 ml/h to 0.8 +/- 0.5 and 0.3 +/- 0.2 ml/h, respectively (N = 19). Water intake induced by carbachol (2 nmol) injected into the MSA was decreased by previous injection of yohimbine (80 nmol) + phenylephrine (160 nmol) and prazosin (40 nmol) + phenylephrine (160 nmol) from 5.4 +/- 1.2 ml/h to 1.0 +/- 0.7 and 1.8 +/- 0.8 ml/h, respectively (N = 16). The cannula reached both the medial septal area in its medial portion and the lateral hypothalamus. It has been suggested that the different pathways for induction of drinking converge on a final common pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of electrolytic and chemical lesion by ibotenic acid of the amygdala on salt intake.

Sodium chloride intake was studied in male Holtzman rats weighing 250-300 g submitted to electrolytic and chemical lesion of the cell bodies, not fibers of the amygdaloid complex. Sodium chloride (1.5%) intake increased in animals with electrolytic lesion of the corticomedial nucleus of the amygdala. Sodium chloride (1.5%) intake increased after ibotenic acid injection into the corticomedial nucleus of the amygdala to a larger extent (26.6 +/- 9.2 to 147.6 +/- 34.6 ml/5 days). The results indicate that sodium intake response can be induced by lesions, which involved only cell bodies. The fibers of passage of the corticomedial nucleus of the amygdala produce a water intake less consistent than that induced by ibotenic acid, which is more acute. The results show that cell bodies of this region of the amygdala are involved in the control of sodium chloride intake.

Effect of electrolytic and chemical lesion by ibotenic acid of the amygdala on salt intake

Sodium chloride intake was studied in male Holtzman rats weighing 250-300 g submitted to electrolytic and chemical lesion of the cell bodies, not fibers of the amygdaloid complex. Sodium chloride (1.5 percent) intake increased in animals with electrolytic lesion of the corticomedial nucleus of the amygdala. Sodium chloride (1.5 percent) intake increased after ibotenic acid injection into the corticomedial nucleus of the amygdala to a larger extent (26.6 + or - 9.2 to 147.6 + or - 34.6 ml/5 days). The results indicate that sodium inake response can be induced by lesions, which involved only cell bodies. The fibers of passage of the corticomedial nucleus of the amygdala produce a water intake less consistent than that induced by ibotenic acid, which is more acute. The results show that cell bodies of this region of the amygdala are involved in the control of sodium chloride intake

Interaction between cholinergic and adrenergic synapses of the rat subfornical organ and the thirst-inducing effect of angiotensin II.

Previous studies by our group and other authors have demonstrated that application of carbachol or angiotensin II to the subfornical organ (SFO) of satiated rats causes an intense thirst-inducing response. It has also been demonstrated that muscarinic cholinergic synapses are mainly involved in the thirst-inducing effect of carbachol, with a secondary role played by nicotinic receptors. The beta-adrenergic pathways of the SFO have also been shown to participate in the regulation of water intake. The present study was designed to investigate the possible interaction between cholinergic and adrenergic neurons of the subfornical organ and the effect of angiotensin II and carbachol in the regulation of water intake by this structure. The intense water intake induced by injection of 2 nmol carbachol into the SFO was markedly reduced when different doses of propranolol (20, 40, 80, and 160 nmol) were previously injected. The response to carbachol, however, was not changed by previous treatment with regitine (20, 40, and 80 nmol). Injection of 0.1 to 4.0 ng angiotensin II into the SFO caused a dose-dependent increase in water intake. When the 4 ng dose of angiotensin was injected into the SFO after an injection of atropine (20, 40, and 80 nmol), complete absence of water intake was observed, the same occurring when propranolol was previously injected at doses of 40 and 80 nmol. The thirst-inducing effect of angiotensin II (4 ng) was not changed by previous injection of hexamethonium (20, 40, 80, and 160 nmol) or phentolamine (20, 40, and 80 nmol). These results permit us to suggest that angiotensin II and carbachol induce thirst when applied to the SFO by acting through independent systems. The participation of beta-adrenergic receptors in the thirst-inducing effect of angiotensin II and carbachol was also demonstrated, as well as the participation of muscarinic cholinergic receptors in the thirst-inducing effect of angiotensin II injected into the SFO.