Role of angiotensin II and vasopressin receptors within the supraoptic nucleus in water and sodium intake induced by the injection of angiotensin II into the medial septal area

In this study we investigated the effects of the injection into the supraoptic nucleus (SON) of non-peptide AT1- and AT2-angiotensin II (ANG II) receptor antagonists, DuP753 and PD123319, as well as of the arginine-vasopressin (AVP) receptor antagonist d(CH2)5-Tyr(Me)-AVP, on water and 3% NaCl intake induced by the injection of ANG II into the medial septal area (MSA). The effects on water or 3% NaCl intake were assessed in 30-h water-deprived or in 20-h water-deprived furosemide-treated adult male rats, respectively. The drugs were injected in 0.5 µl over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. Antagonists were injected at doses of 20, 80 and 180 nmol. Water and sodium intake was measured over a 2-h period. Previous administration of the AT1 receptor antagonist DuP753 into the SON decreased water (65%, N = 10, P<0.01) and sodium intake (81%, N = 8, P<0.01) induced by the injection of ANG II (10 nmol) into the MSA. Neither of these responses was significantly changed by injection of the AT2-receptor antagonist PD123319 into the SON. on the other hand, while there was a decrease in water intake (45%, N = 9, P<0.01), ANG II-induced sodium intake was significantly increased (70%, N = 8, P<0.01) following injection of the V1-type vasopressin antagonist d(CH2)5-Tyr(Me)-AVP into the SON. These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Furthermore, they do not support the involvement of MSA AT2 receptors in the mediation of these responses.

Baclofen into the lateral parabrachial nucleus induces hypertonic sodium chloride and sucrose intake in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Lateral parabrachial nucleus and central amygdala in the control of sodium intake

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Moxonidine into the lateral parabrachial nucleus reduces renal and hormonal responses to cell dehydration

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Estrous behavior and the estrus-to-ovulation interval in Nelore cattle (Bos indicus) with natural estrus or estrus induced with prostaglandin F2 alpha or norgestomet and estradiol valerate

Estrous behavior and the estrus-to-ovulation interval are essential for estimating the best time to artificially inseminate cattle. Because these parameters are not well characterized in the Nelore breed (Bos indicus), the main purpose of the this study was to determine the estrus-to-ovulation interval in Nelore heifers and cows with natural estrus or with estrus induced by treatments with PGF2 alpha or norgestomet and estradiol valerate (NEV). The cows and heifers were observed continuously (24 h a day) to determine the onset of estrus and to study estrous behavior in the cows. Ten hours after the start of estrus the ovaries were scanned every 2 h by ultrasonography to monitor the dominant follicle until ovulation. Blood samples were collected periodically to determine progesterone levels by RIA. Administration of PGF2 alpha (2 injections, 11 days apart) did not induce estrus in most Nelore females in spite of the presence of functional CL, indicated by progesterone concentrations above 6.0 ng/ml in 25 of 28 animals. Treatment with NEV induced high sexual receptivity in cows (10/11), but only 66% ovulated. Cows with natural or induced estrus exhibited behavioral estrus of 10.9 +/- 1.4 h, and ovulation occurred 26.6 +/- 0.44 h (n = 26) after the onset of estrus. In most of the cows (53.8%) estrus began at night (between 1801 and 600 h), and 34.6% it started and finished during the night. It is concluded that in Nelore females ovulation occurs approximately 26 h after the onset of estrus. Additionally, estrous behavior is shorter than in European breeds, and there is a high incidence of estrus at night, which makes it difficult to detect and, consequently, impairs Al in Nelore cattle. The observation that a high percentage of Nelore females with an active CL did not respond to usual dosages of PGF2 alpha warrants further investigation. (C) 1998 by Elsevier B.V.

Orchidectomy enhances the effects of phenylephrine in rat isolated portal vein

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Discretizing the deformation parameter in the su(q)(2) quantum algebra

Inspired in recent works of Biedenham [1, 2] on the realization of the q-algebra su(q)(2), We show in this note that the condition [2j + 1](q) = N-q(j) = integer, implies the discretization of the deformation parameter alpha, where q = e(alpha). This discretization replaces the continuum associated to ct by an infinite sequence alpha(1), alpha(2), alpha(3),..., obtained for the values of j, which label the irreps of su(q)(2). The algebraic properties of N-q(j) are discussed in some detail, including its role as a trace, which conducts to the Clebsch-Gordan series for the direct product of irreps. The consequences of this process of discretization are discussed and its possible applications are pointed out. Although not a necessary one, the present prescription is valuable due to its algebraic simplicity especially in the regime of appreciable values of alpha.

Thermal behavior of Cu-Al alloys near the alpha-Cu-Al solubility limit

The thermal behavior of Cu-Al alloys with 17, 19 and 21 at.%Al was examined by differential thermal analysis (DTA), differential scanning calorimetry (DSC), X-ray diffractometry (XRD), optical microscopy (OM) and scanning electron microscopy (SEM). The presence of the gamma phase (Al4Cu9) was clearly detected for the Cu-19 at.%Al alloy and caused the alpha (2) phase disordering process in two stages. The tendency to increase the alpha (2) dissolution precipitates with the increase in the Al content seems to be reverted for compositions at about 21 at.%Al and the heating/cooling ratio seems to influence the thermal response of this process. The presence of the endothermic peak corresponding to the beta (1)--> beta transformation depends on an incomplete beta decomposition reaction. The variation of the heating rate showed that the beta (1)-->(alpha+gamma (1)) decomposition is the dominant reaction for alloys containing 19 and 21 at.%Al.

CARDIOVASCULAR EFFECTS OF CENTRAL CLONIDINE IN CONSCIOUS RATS AFTER HYPOTHALAMIC-LESIONS

The central injection of clonidine (an alpha-2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions in the anteroventral third ventricle (AV3V) region or in the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by central clonidine in rats. Mean arterial pressure and heart rate were recorded in sham or AV3V-lesioned rats with cerebral stainless steel cannulae implanted into the lateral cerebral ventricle (ICV) or LH. and in sham or bilateral LH-lesioned rats with cannulae-implanted ICV. The injection of clonidine (40 nmol) ICV or into the LH of sham rats produced a pressor response (37 +/- 2-48 +/- 3 mmHg) and bradycardia (-45 +/- 10--93 +/- 6 bpm). After AV3V-lesion (3 and 12 days) or LH-lesion (3 days) the pressor response was abolished and a small hypotensive response was induced by the injection of clonidine (-1 +/- 3--16 +/- 3 mmHg). The bradycardia (-27 +/- 6--57 +/- 11 bpm) was reduced, but not abolished by the lesions. These results show that the AV3V region and LH are important cerebral structures that participate in the excitatory pathways involved in the pressor response to central clonidine in rats. They also suggest that, in the absence of these pressor pathways, the hypotensive responses to central clonidine may appear in conscious rats.

LESIONS OF THE LATERAL HYPOTHALAMUS IMPAIR THE PRESSOR-RESPONSE TO CLONIDINE INJECTED INTO THE MEDIAL SEPTAL AREA OF CONSCIOUS RATS

The central injection of clonidine (an alpha-2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions of the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by clonidine injected into the medial septal area (MSA) in conscious and unrestrained rats. Male Holtzman rats weighing 250-300 g were used. Mean arterial pressure and heart rate were recorded in sham- or bilateral LH-lesioned rats with a cerebral stainless steel cannula implanted into the MSA. The injection of clonidine (40 nmol/mu-l) into the MSA of sham rats (N = 8) produced a pressor response (36 +/- 7 mmHg, P<0.05) and bradycardia (-70 +/- 13 bpm, P<0.05) compared to saline. Fourteen days after LH-lesion (N = 9) the pressor response was reduced (9 +/- 10 mmHg, P<0.05) but no change was observed in the bradycardia (-107 +/- 24 bpm). These results show that LH is an important area involved in the pressor response to clonidine injected into the MSA of rats.

Idazoxan and the effect of intracerebroventricular oxytocin or vasopressin on sodium intake of sodium-depleted rats

The alpha(2)-adrenergic agonist clonidine and the neuropeptide oxytocin, inhibit sodium intake when injected intracerebroventricularly (i.c.v.). The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. injection of idazoxan, an alpha(2)-adrenergic antagonist. Clonidine (30 nmol), oxytocin (40, 80 nmol) and vasopressin (40, 80 nmol) were injected i.c.v. 20 min prior to a 1.5% NaCl appetite test, in rats depleted of sodium for 24 h by a combination of a single s.c. injection of furosemide (10 mg/rat) and removal of ambient sodium. Every dose of clonidine, oxytocin and vasopressin inhibited the 1.5% NaCl intake. Seizures were observed with the higher dose of vasopressin, but not with either dose of oxytocin. The effect of i.c.v. injection of clonidine (30 nmol), oxytocin (80 nmol) or vasopressin (40 nmol) was partially inhibited by prior i.c.v. injection of idazoxan (160, 320 nmol). The results suggest that the inhibition of 1.5% NaCl intake induced by i.c.v. injection of neuropeptides in sodium-depleted rats depends, in part, on the activation of central alpha(2)-adrenoceptors. (C) 1997 Elsevier B.V. B.V. All rights reserved.

Antagonism of clonidine injected intracerebroventricularly in different models of salt intake

Clonidine, an alpha 2-adrenergic agonist, injected into the brain inhibits salt intake of animals treated by the diuretic model of sodium depletion. In the present study, we address the question of whether central injection of clonidine also inhibits salt intake in animals deprived of water or in the need-free state. Saline or clonidine (30 nmol) was injected into the anterior third ventricle of 24-h sodium-depleted (furosemide + removal of ambient sodium), of 24-h water-deprived and of normovolemic (need-free state) adult male rats, Clonidine injected intracerebroventricularly (icv) inhibited the 1.5% NaCl intake for 120 min by 50 to 90% in every model tested. Therefore, different models of salt intake are inhibited by icv injection of clonidine, Idazoxan, an alpha 2-adrenergic antagonist, injected icy at a dose of 160 nmol, inhibited the effect of clonidine only in the furosemide + removal of ambient sodium model of salt intake. This indicates that the antagonism of this effect by idazoxan is dependent on the body fluid/sodium status of the animal.

ANTINOCICEPTIVE EFFECT OF AMITRAZ IN MICE AND RATS

Amitraz, a formamidine insecticide and acaricide used in veterinary practice, presents side effects related to its pharmacological activity on az-adrenergic receptors. The present study was undertaken to investigate the antinociceptive effect of amitraz in rats and mice. The tail-flick test was used to determine the duration of the antinociceptive effect of the intraperitoneal tip) administration of amitraz (1 and 2 mg/kg, 10 animals per group) in male Wistar rats weighing 180-220 g. The writhing test (using 10 ml/kg of a 0.6% acetic acid solution as a painful stimulus). was performed in 140 male Swiss mice weighing 20-30 g, divided into 14 groups that received ip injections of saline, amitraz (0.5, 1.0, 1.5, 2.0 and 4.0 mg/kg), xylazine or detomidine (1.0, 1.5, 2.0 and 4.0 mg/ kg), in order to compare the effect of amitraz to that caused by xylazine and detomidine, and to investigate the participation of alpha(2)-adrenergic receptors which were blocked by idazoxan (1 mg/kg). Amitraz induced a significant antinociceptive effect in both rats and mice. This effect is blocked in mice by idazoxan.

Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats

We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and presser responses induced by the concomitant angiotensinergic, alpha(2) and beta adrenergic activation of the MnPO, whereas alpha(1) activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.

Nitric oxide and anglotensin II receptors mediate the pressor effect of angiotensin II: A study in conscious and zoletil-anesthetized rats

The circumventricular structures of the central nervous system and nitric oxide are involved in arterial blood pressure control, and general anesthesia may stimulate the central renin-angiotensin system. We therefore investigated the central role of angiotensin 11 and nitric oxide on the regulation of systemic arterial blood pressure in conscious and anesthetized rats. METHODS: Rats with stainless steel cannulae implanted into their lateral ventricle were studied. We injected the AT(1) and AT(2) angiotensin 11 receptor antagonists, losartan and PD123319, L-NAME, 7-nitroindazole (nitric oxide synthetase inhibitors), and FK409 (nitric oxide donor agent) into the lateral ventricles. Mean arterial blood pressure (MAP) was recorded in conscious and zoletil-anesthetized rats. RESULTS: Mean +/- (SEM) baseline MAP was 117.5 +/- 2 mm Hg. Angiotensin II injected into the brain lateral ventricle increased MAP from 136.5 +/- 2 min Hg to 138.5 +/- 4 mm Hg (Delta 16 +/- 3 mm Hg to Delta 21 +/- 3 mm Hg) for all experimental groups versus control from 116 +/- 2 mm Hg to 120 +/- 3 mm Hg (Delta 3 +/- 1 mm Hg to A5 +/- 2 mm Hg) (P < 0.05). L-NAME or 7-nitroindazole enhanced the angiotensin II pressor effect (P < 0.05). Prior injection of losartan and PD123319 decreased the angiotensin 11 pressor effect and the enhancement effect of L-NAME and 7-nitroindazole (P < 0.05). Zoletil anesthesia did not interfere with the effects of angiotensin 11, AT,, AT2 antagonists, or nitric oxide synthetase inhibitors. CONCLUSIONS: Endogenous nitric oxide functions tonically as a central inhibitory modulator of the angiotensinergic system. AT, and AT2 receptors influence the angiotensin 11 central control of arterial blood pressure. Zoletil anesthesia did not interfere with these effects. (Anesth Analg 2007;105:1293-7)