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Extracellular volume expansion (EVE) was performed in intact rats and 24 h after locus coeruleus (LC) lesions or sham-operation. Blood pressure was registered 5 min before and after EVE. At the end of the experiment the animals were decapitated and blood was collected from the trunk for quantification of plasma atrial natriuretic peptide (ANP). All experimental groups showed similar basal blood pressure. Volume expansion caused a slight decrease in blood pressure and an increase in ANP secretion in all groups, but these changes were significantly enhanced in animals bearing a lesion in the anterior region of the LC. There was no pronounced c-fos expression in any region of the LC 2 h after EVE in intact animals. In conclusion, the data support the idea that the LC does not participate in blood pressure control in resting conditions. However, the anterior region of the LC seems to play a role when adjustments of blood pressure and excretion of water and sodium are necessary during changes in blood volume. The results on c-fos expression are in accordance with the idea that this nucleus may be part of an inhibitory pathway which modulates the circuits of control for depressor reflex response and ANP secretion after extracellular volume expansion.

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Injection of acetylcholine (ACh) (2.5-60 nmol) into the anterior cingulate cortex caused dose-dependent hypotensive responses (Emax = -25.3 mmHg) and no change in the heart rate. The hypotensive response to 30 nmol of ACh was blocked by local pretreatment with atropine (3 nmol) or 4-DAMP (6.7 nmol), a non-tropine muscarinic antagonist. When the same dose of atropine was injected i.v., no changes were observed in the hypotensive response to intracortical ACh. This observation rules out the possible leakage of ACh into the peripheral circulation and favors the idea of a cortical site of action. The injection of the same dose of ACh into the corpus callosum or the occipital cortex did not cause changes in the cardiovascular system. The present results confirm earlier evidence that the cingulate cortex is involved in the control of the autonomic system and indicate that cholinergic muscarinic receptors in the cingulate cortex mediate a hypotensive response without a change in heart rate.

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Bilateral electrolytic lesions in the rat Locus Coeruleus (LC) were made one or seven days before experimentation. Four hemorrhage sessions, withdrawing 10% of the blood volume per session, were performed in 5 min intervals in freely moving rats. Blood pressure (BP) was not affected by the lesions and did not drop in the first, but decreased in all subsequent hemorrhages. The decrease in BP in animals with lesion in the anterior LC was similar to the controls. However, animals with lesions in the posterior LC showed an enhanced decrease in BP during the second hemorrhage, in acute and chronic experiments. Expression of Fos protein was studied to investigate the relationship between LC activity and BP changes. Two hours after the second hemorrhage, the brains were removed and processed for Fos immunocytochemistry. Hemorrhage increased the number of Fos immunoreactive neurons mainly in the posterior LC. We conclude that (1) the LC does may not play a role in cardiovascular control during resting, but seems to mediate compensatory cardiovascular mechanisms in situations of hypovolemia; and (2) the posterior LC, but not the anterior, plays a pressor role during hemorrhage.

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The intracerebroventricular (i.c.v.) administration of noradrenaline (NA) caused dose-dependent blood pressure increases in unanesthetized rats with an ED50 of 35 nmol. Similar pressor responses were observed after the i.c.v. injection of the more selective alpha 1-agonists ST-91, methoxamine and phenylephrine with ED50 of 60, 155 and 575 nmol, respectively. The maximal pressor response was 57 +/- 3 mmHg. No tachyphylaxis was observed when injections of 37.5 nmol of NA was i.c.v.-injected at an interval of 24 hr. No significant differences were observed in the plasma content of NA and adrenaline at the peak of the pressor response to i.c.v.-injected NA when compared to i.c.v. injections of saline. The pressor effects of NA were blocked by the i.c.v. pretreatment with prazosin or yohimbine with ID50 of 0.9 and 29 nmol, respectively. Prazosin was 32-fold more potent than yohimbine in blocking the effect of i.c.v. NA, suggesting the involvement of alpha 1-adrenoceptors in the central mediation of the pressor response to NA. Intravenous injections of 13 nmol of prazosin or 90 nmol of yohimbine did not affect the pressor response to i.c.v. NA, further indicating the central nervous system nature of the response.

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Injections of acetylcholine (ACh) into the lateral septal area (LSA) caused blood pressure increases in unanesthetized freely moving rats. ACh was injected in the dose range of 0.1-54 nmol/500 nl using regular metal needles (200 microns o.d.). In the LSA, injections of carbachol or ACh (2.5 nmol/500 nl) were equipotent (+22 +/- 2 and +19 +/- 3 mmHg, respectively) suggesting the existence of an ACh-sensitive pressor site in the LSA. Maximum responses to ACh injected either intracerebroventricularly (i.c.v.) or into the LSA were not significantly different (+23 +/- 1 and +21 +/- 2 mmHg, respectively). However, the ED50 for the injection into the LSA (0.24 nmol) was significantly lower than that observed after i.c.v. injection (2.6 nmol), ruling out a possible leakage of ACh from the LSA and into the ventricular space. This idea is supported by data showing that the effect of the intraseptal injection of 30 nmol of ACh was blocked by pretreatment with 3 nmol of atropine either i.c.v. or into the LSA, whereas the effects of i.c.v. ACh were completely blocked by i.c.v. atropine, but only partially (42%) when atropine was injected into the LSA. The idea of the existence of an ACh-sensitive site in the LSA is further supported by the more direct observation that injections of 30 nmol/100 nl of ACh into the LSA using glass needles (50-70 microns o.d.) caused similar pressor responses. Neither the i.v. pretreatment with pentolinium or adrenalectomy affected the response to 30 nmol/500 nl of ACh injected into the LSA, ruling out the involvement of the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

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1. The injection of 13.5-54 nmol/500 nl of acetylcholine (ACH) into different brain areas of unanesthetized freely-moving 200-250 g male Wistar rats caused only pressor responses. 2. In the prosencephalon, the lateral septal area was the site at which ACH was more effective, whereas injections into surrounding areas, such as the accumbens/bed nucleus striae terminalis, the medial septal area or the lateral ventricle were less effective. No blood pressure effects were observed after injection into the anterior amygdala. 3. In the diencephalon, the ventromedial hypothalamic nucleus was the most sensitive site, whereas injection of ACH into surrounding areas, such as the posterior and lateral hypothalamic or the dorsal and ventral premammillary nuclei was less effective. 4. At all sites tested, the local pretreatment with 138-276 nmol atropine abolished the pressor response to ACH, suggesting a mediation through muscarinic receptors. 5. The sites of injection were confirmed histologically. 6. The present data indicate the existence of a cholinergic-sensitive site involved in the control of blood pressure at the level of the lateral septal area.

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The injection of 13.5-54 nmol/500 nl of acetylcholine (ACH) into different brain areas of unanesthetized freely-moving 200-250 g male Wistar rats caused only pressor responses. In the prosencephalon, the lateral septal area was the site at which ACH was more effective, whereas injections into surrounding areas, such as the accubens/bed nucleus striae terminalis, the medial septal area or the lateral ventricle were less effective. No effective. No blood pressure effects were observed after injection into the anterior amygdala. In the diencephalon, the ventromedial hypothalamic nucleus was the most sensitive site, whereas injection of ACH into surrounding areas, such as the posterior and lateral hypothalamic or the dorsal and ventral prtemammillary nuclei was less effective. At all sites tested, the local pretreatment with 138-276 nmol atropine abolished the pressor response to ACH, suggesting a mediation through muscarinic receptors. The sites of injection were confirmed histologically. The present data indicate the existence of a cholinergic-sensitive site involved in the control of blood pressure at the level of the lateral septal area

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Microinjections of catecholamines were performed into the lateral ventricle of anesthetized and unanesthetized rats and the blood pressure effects recorded prior to or after the administration of pharmacological antagonists. Injections of 20-100 micrograms normetanephrine (alpha-agonist) produced only pressor responses in both groups of animals. Injections of 10-20 micrograms of norepinephrine (preferentially an alpha-agonist) produced mainly pressor in awake and only depressor responses in anesthetized animals, whereas injections of 10-20 micrograms of epinephrine (preferentially a beta-agonist) produced only depressor responses in both groups of animals. Intracerebroventricular pretreatment with the beta-blocker propranolol (40-100 micrograms) blocked the depressor responses to the catecholamines or even reverted them into clear pressor response. Pretreatment with the alpha-blocker phentolamine (100 micrograms) reduced the pressor effects induced by the intraventricular injection of catecholamines. The existence of central alpha-pressor and beta-depressor mechanisms mediating the blood pressure responses to the intracerebroventricular administration of catecholamines is proposed.

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Catecholamines administered intracerebroventricularly (i.c.v.) have cardiovascular effects mediated by the CNS. Although hypotension constitutes the more prominent response, an increase in blood pressure has also been reported after the intracerebroventricular injection of these amines. Anaesthesia interferes with pressor responses mediated by the CNS to a larger extent than with depressor mechanisms and constitutes one of the major factors influencing the pattern of response to the amines. The depressor response observed after the intracerebroventricular administration of noradrenaline is reversed into increases in blood pressure in awake animals. In the present experiment, the action of intracerebroventricularly injected noradrenaline was compared in anaesthetized and conscious rats. The results indicated that the pressor response in awake rats was not mediated by the sympathetic nervous system and involved the release of a pituitary humoral-factor, most probably vasopressin, whereas the depressor response observed in anaesthetized animals was not dependent on pituitary mediation. The involvement of histaminergic mechanisms in the CNS in the control of the pressor response to intracerebroventricularly administered noradrenaline in the rat is proposed.

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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.

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Isoprenaline was microinjected into the cerebroventricular spaces of anesthetized or unanesthetized rats and the blood pressor effects recorded prior to or after intraventricular administration of pharmacologic antagonists. Injection of 1-20 micrograms of isoprenaline produced only depressor responses in both groups of animals. Pretreatment with 400-200 micrograms of propranolol partially antagonized the depressor effect of isoprenaline, whereas pretreatment with 40 micrograms of phenoxybenzamine or 100 micrograms phentolamine potentiated the depressor response to isoprenaline. The involvement of central beta-adrenoceptors and a propranolol-insensitive mechanism in the depressor response to intracerebroventricular isoprenaline is proposed. Indirect evidence of a central alpha-adrenoceptor mediation of pressor mechanisms counteracting the depressor responses elicited by beta-adrenoceptor stimulation is presented.

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