Changes in sodium appetite evoked by lesions of the commissural nucleus of the tractus solitarius

Ablation of the area postrema/caudal nucleus of the tractus solitarius (NTS) complex increases sodium intake, but the effect of selective lesions of the caudal NTS is not known. We measured depletion-induced sodium intake in rats with electrolytic lesions of the commissural NTS that spared the area postrema. One day after the lesion, rats were depleted of sodium with furosemide (10 mg/kg body weight, sc) and then had access to water and a sodium-deficient diet for 24 h when 1.8% NaCl was offered. Water and saline intakes were measured for 2 h. Saline intake was higher in lesioned than in sham-lesioned rats (mean ± SEM: 20 ± 2 vs 11 ± 3 mL/2 h, P < 0.05, N = 6-7). Saline intake remained elevated in lesioned rats when the tests were repeated 6 and 14 days after the lesion, and water intake in these two tests was increased as well. Water intake seemed to be secondary to saline intake both in lesioned and in sham-lesioned rats. A second group of rats was offered 10% sucrose for 2 h/day before and 2, 7, and 15 days after lesion. Sucrose intake in lesioned rats was higher than in sham-lesioned rats only 7 days after lesioning. A possible explanation for the increased saline intake in rats with commissural NTS lesions could be a reduced gastrointestinal feedback inhibition. The commissural NTS is probably part of a pathway for inhibitory control of sodium intake that also involves the area postrema and the parabrachial nucleus.Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de FisiologiaFaculdade de Medicina do ABC Departamento de FisiologiaUNIFESP, EPM, Depto. de FisiologiaSciEL

Cardiovascular adjustments induced by hypertonic saline in hemorrhagic rats: Involvement of carotid body chemoreceptors

The peripheral hyperosmolarity elicited by intravenous infusion of hypertonic saline brings potential benefits to the treatment of hemorrhage. the neural mechanisms involved in these beneficial effects remain unknown. the present study examines the role of carotid chemoreceptors in cardiovascular responses induced by hypertonic saline after hypovolemic hemorrhage in rats. Male Wistar rats (300-400 g) were anesthetized with thiopental, and instrumented for recording of mean arterial pressure. Arterial pressure was reduced to 60 mm Hg by withdrawal of arterial blood over 10 min, and maintained at this level for 60 min by withdrawal or infusion of blood. in control rats (n = 8) with intact chemoreceptors, the subsequent intravenous infusion of hypertonic saline (3M NaCl, 1.8 ml kg(-1) body weight, in 2 min) restored blood pressure (pressure increased from 61 +/- 4 to 118 +/- 5 mm Hg). in experimental rats (n = 8), the carotid body arteries were tied, 30 min after the beginning of the hypotensive phase, leaving the carotid chemoreceptors ischemic. in these rats, hypertonic saline failed to restore blood pressure (pressure increased from 55 +/- 1 to 70 +/- 6 mm Hg). These findings suggest that the restoration of blood pressure after hypovolemic hemorrhage induced by hypertonic saline depends on intact carotid chemoreceptors. (C) 2010 Elsevier B.V. All rights reserved.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ Fed Goias, Dept Physiol Sci, Inst Ciencias Biol 2, BR-74001970 Goiania, Go, BrazilUniversidade Federal de São Paulo, Dept Physiol, Escola Paulista Med, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, Escola Paulista Med, São Paulo, BrazilCAPES: BEX1380/07-9Web of Scienc

Cardiovascular Responses Induced by Obstructive Apnea Are Enhanced in Hypertensive Rats Due to Enhanced Chemoreceptor Responsivity

Spontaneously hypertensive rats (SHR), like patients with sleep apnea, have hypertension, increased sympathetic activity, and increased chemoreceptor drive. We investigated the role of carotid chemoreceptors in cardiovascular responses induced by obstructive apnea in awake SHR. A tracheal balloon and vascular cannulas were implanted, and a week later, apneas of 15 s each were induced. the effects of apnea were more pronounced in SHR than in control rats (Wistar Kyoto; WKY). Blood pressure increased by 57 +/- 3 mmHg during apnea in SHR and by 28 +/- 3 mmHg in WKY (p < 0.05, n = 14/13). the respiratory effort increased by 53 +/- 6 mmHg in SHR and by 34 +/- 5 mmHg in WKY. the heart rate fell by 209 +/- 19 bpm in SHR and by 155 +/- 16 bpm in WKY. the carotid chemoreceptors were then inactivated by the ligation of the carotid body artery, and apneas were induced two days later. the inactivation of chemoreceptors reduced the responses to apnea and abolished the difference between SHR and controls. the apnea-induced hypertension was 11 +/- 4 mmHg in SHR and 8 +/- 4 mmHg in WKY. the respiratory effort was 15 +/- 2 mmHg in SHR and 15 +/- 2 mmHg in WKY. the heart rate fell 63 +/- 18 bpm in SHR and 52 +/- 14 bpm in WKY. Similarly, when the chemoreceptors were unloaded by the administration of 100% oxygen, the responses to apnea were reduced. in conclusion, arterial chemoreceptors contribute to the responses induced by apnea in both strains, but they are more important in SHR and account for the exaggerated responses of this strain to apnea.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, BrazilFAPESP: 2010/19705-6CNPq: 472187/2010-4Web of Scienc

Repeated amygdala-kindled seizures induce ictal rebound tachycardia in rats

It is thought that cardiovascular changes may contribute to sudden death in patients with epilepsy. To examine cardiovascular alterations that occur during epileptogenesis, we measured the heart rate of rats submitted to the electrical amygdala kindling model. Heart rate was recorded before, during, and after the induced seizures. Resting heart rate was increased in stages 1, 3, and 5 as compared with the unstimulated control condition. in the initial one third of the seizures, we observed bradycardia, which increased in intensity with increasing stage and was blocked by injecting methyl atropine. During stage 5 seizures, a rebound tachycardia was observed that also increased in intensity with increasing number of seizures. This study demonstrated the influence of seizure frequency on cardiac autonomic modulation, providing a basis for discussion of potential mechanisms that cause patients with epilepsy to die suddenly. (C) 2011 Elsevier Inc. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo, Dept Neurol Neurosci, São Paulo, BrazilUniv Fed Goias, Dept Physiol Sci, Goiania, GO, BrazilUniversidade Federal de São Paulo, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol Neurosci, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, São Paulo, BrazilWeb of Scienc

Efferent Pathways in Sodium Overload-Induced Renal Vasodilation in Rats

Hypernatremia stimulates the secretion of oxytocin (OT), but the physiological role of OT remains unclear. the present study sought to determine the involvement of OT and renal nerves in the renal responses to an intravenous infusion of hypertonic saline. Male Wistar rats (280-350 g) were anesthetized with sodium thiopental (40 mg. kg(-1), i.v.). A bladder cannula was implanted for collection of urine. Animals were also instrumented for measurement of mean arterial pressure (MAP) and renal blood flow (RBF). Renal vascular conductance (RVC) was calculated as the ratio of RBF by MAP. in anesthetized rats (n = 6), OT infusion (0.03 mu g . kg(-1), i.v.) induced renal vasodilation. Consistent with this result, ex vivo experiments demonstrated that OT caused renal artery relaxation. Blockade of OT receptors (OXTR) reduced these responses to OT, indicating a direct effect of this peptide on OXTR on this artery. Hypertonic saline (3 M NaCl, 1.8 ml . kg(-1) b.wt., i.v.) was infused over 60 s. in sham rats (n = 6), hypertonic saline induced renal vasodilation. the OXTR antagonist (AT; atosiban, 40 mu g . kg(-1) . h(-1), i.v.; n = 7) and renal denervation (RX) reduced the renal vasodilation induced by hypernatremia. the combination of atosiban and renal denervation (RX+AT; n = 7) completely abolished the renal vasodilation induced by sodium overload. Intact rats excreted 51% of the injected sodium within 90 min. Natriuresis was slightly blunted by atosiban and renal denervation (42% and 39% of load, respectively), whereas atosiban with renal denervation reduced sodium excretion to 16% of the load. These results suggest that OT and renal nerves are involved in renal vasodilation and natriuresis induced by acute plasma hypernatremia.Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ Fed Goias, Ctr Neurosci & Cardiovasc Physiol, Inst Biol Sci, Dept Physiol Sci, Goiania, Go, BrazilUniv Fed Uberlandia, Fac Phys Educ, Inst Biol Sci, BR-38400 Uberlandia, MG, BrazilUniversidade Federal de São Paulo, Dept Physiol, São Paulo, BrazilUniv Fed Goias, Inst Biol Sci, Mol Biol Lab, Goiania, Go, BrazilUniv Fed Goias, Inst Biol Sci, Dept Biochem & Mol Biol, Goiania, Go, BrazilUniversidade Federal de São Paulo, Dept Physiol, São Paulo, BrazilFundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 2012/0055431086Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 2009/10267000352CNPq: 477832/2010-5CNPq: 483411/2012-4Web of Scienc

Ablation of NK1 receptor bearing neurons in the nucleus of the solitary tract blunts cardiovascular reflexes in awake rats

The nucleus of the solitary tract (NTS) receives primary afferents involved in cardiovascular regulation. We investigated the role of NK1-receptor bearing neurons in the NTS on cardiovascular reflexes in awake rats fitted with chronic venous and arterial cannulae. These neurons were lesioned selectively with saporin conjugated with substance P (SP-SAP, 2 mu M, bilateral injections of 20 nL in the subpostremal NTS, or 200 nL in both the subpostremal and the commissural NTS). Before, and 7 and 14 days after injection of SP-SAP, we measured changes in blood pressure and heart rate induced by i.v. injection of phenylephrine and nitroprusside (baroreceptor reflex), cyanide (arterial chemoreceptor reflex), and phenylbiguanide (Bezold-Jarisch reflex). the smaller injections with SP-SAP completely abolished NK1 receptor staining in the subpostremal NTS. the larger injections abolished NK1 receptor immunoreactivity in an area that extended from the commissural NTS to the rostral end of the subpostremal NTS. the lesions seemed to affect only a limited number of neurons, since neutral red stained sections did not show any obvious reduction in cell number. the smaller lesions reduced the gain of baroreflex bradycardia and the hypotension induced by phenylbiguanide. the larger lesions completely abolished the response to phenylbiguanide, blocked the baroreflex bradycardia induced by phenylephrine, severely blunted the baroreflex tachycardia, and blocked the bradycardia and reduced the hypertension induced by cyanide. Thus, these responses depend critically on NK1-receptor bearing neurons in the NTS. (c) 2006 Elsevier B.V. All rights reserved.Universidade Federal de São Paulo, Dept Fisiol, EPM, BR-04023062 São Paulo, BrazilUniv Estadual Paulista, Fac Odontol, Dept Physiol, BR-14801903 Araraquara, SP, BrazilUniversidade Federal de São Paulo, Dept Fisiol, EPM, BR-04023062 São Paulo, BrazilWeb of Scienc