Lesions in lateral parabrachial nucleus enhance drinking to angiotensin II and isoproterenol

Ohman, Lynne E.; Johnson, A. Tim

doi:10.1152/ajpregu.1986.251.3.r504

Cited by 53 publications

(49 citation statements)

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“…The overdrinking observed in commNTSlesioned rats after sc isoproterenol was similar to that observed in studies using LPBN (3,7) and AP (12) lesions. Considering the anatomical connections among these areas and the behavioral data, it seems that the commNTS is also part of the hindbrain inhibitory pathways involved in the control of water intake.…”

Section: Discussionsupporting

confidence: 86%

“…Besides, AP/mNTS lesions increase daily ad libitum intake of hypertonic sodium solution (1) and enhance consumption of concentrated saline solution (3% NaCl) during the first few hours after presentation of saline to sodium-repleted rats (31). Therefore, it is possible that projections from the AP/mNTS to the LPBN are involved in the control of water and sodium intake (1)(2)(3)(4)(5)7,(10)(11)(12)31), while, as suggested by the present data, the commNTS is involved only in the control of water intake.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have demonstrated that the hindbrain is involved in the inhibitory control of water intake and salt appetite, in contrast to forebrain areas, that mainly exert an excitatory drive on water and sodium intake (1)(2)(3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

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Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

Blanch

Freiria-Oliveira

Colombari

et al. 2007

Braz J Med Biol Res

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The nucleus of the solitary tract (NTS) is the primary site of the cardiovascular afferent information about arterial blood pressure and volume. The NTS projects to areas in the central nervous system involved in cardiovascular regulation and hydroelectrolyte balance, such as the anteroventral third ventricle region and the lateral parabrachial nucleus. The aim of the present study was to investigate the effects of electrolytic lesion of the commissural NTS on water and 0.3 M NaCl intake and the cardiovascular responses to subcutaneous injection of isoproterenol. Male Holtzman rats weighing 280 to 320 g were submitted to sham lesion or electrolytic lesion of the commissural NTS (N = 6-15/group). The sham-lesioned rats had the electrode placed along the same coordinates, except that no current was passed. Water intake induced by subcutaneous isoproterenol (30 µg/kg body weight) significantly increased in chronic (15 days) commissural NTS-lesioned rats (to 2.4 ± 0.2 vs sham: 1.9 ± 0.2 mL 100 g body weight -1 60 min -1 ). Isoproterenol did not induce any sodium intake in sham or in commissural NTS-lesioned rats. The isoproterenol-induced hypotension (sham: -27 ± 4 vs commissural NTS-lesioned rats: -22 ± 4 mmHg/20 min) and tachycardia (sham: 168 ± 10 vs commissural NTS: 144 ± 24 bpm/20 min) were not different between groups. The present results suggest that the commissural NTS is part of an inhibitory neural pathway involved in the control of water intake induced by subcutaneous isoproterenol, and that the overdrinking observed in lesioned rats is not the result of a cardiovascular imbalance in these animals.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

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Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

Blanch

Freiria-Oliveira

Colombari

et al. 2007

Braz J Med Biol Res

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“…Electrolytic or neurotoxic (ibotenic acid) lesions of the LPBN increase water intake induced by subcutaneous ANG II or isoproterenol or intracerebroventricular ANG II in rats (15,42,43). Bilateral LPBN injections of methysergide strongly increase water and 0.3 M NaCl intake induced by icv ANG II or by treatment with subcutaneous injections of furosemide combined with a low dose of the angiotensin-converting enzyme inhibitor captopril (40), but have no effect on drinking or sodium intake when animals are satiated and normovolemic (39,40).…”

Section: Discussionmentioning

confidence: 99%

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

Margatho

Giusti‐Paiva²,

Menani³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This study investigated the involvement of serotonergic mechanisms of the lateral parabrachial nucleus (LPBN) in the control of sodium (Na ϩ ) excretion, potassium (K ϩ ) excretion, and urinary volume in unanesthetized rats subjected to acute isotonic blood volume expansion (0.15 M NaCl, 2 ml/100 g of body wt over 1 min) or control rats. Plasma oxytocin (OT), vasopressin (VP), and atrial natriuretic peptide (ANP) levels were also determined in the same protocol. Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In rats treated with vehicle in the LPBN, blood volume expansion increased urinary volume, Na ϩ and K ϩ excretion, and also plasma ANP and OT. Bilateral injections of serotonergic receptor antagonist methysergide (1 or 4 g/200 l) into the LPBN reduced the effects of blood volume expansion on increased Na ϩ and K ϩ excretion and urinary volume, while LPBN injections of serotonergic 5-HT2a/HT2c receptor agonist, 2.5-dimetoxi-4-iodoamphetamine hydrobromide (DOI; 1 or 5 g/200 l) enhanced the effects of blood volume expansion on Na ϩ and K ϩ excretion and urinary volume. Methysergide (4 g) into the LPBN decreased the effects of blood volume expansion on plasma ANP and OT, while DOI (5 g) increased them. The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion. serotonin; natriuresis; atrial natriuretic peptide; oxytocin; vasopressin ISOTONIC BLOOD VOLUME expansion, by reflex mechanisms, induces a series of regulatory responses, including the inhibition of the sympathetic outflow to the kidney, heart, and blood vessels, reduction of renin and vasopressin (VP) secretion, and increase in the levels of circulating atrial natriuretic peptide (ANP) and oxytocin (OT) that leads to diuresis and natriuresis (1,2,12,14,20,24,45,53).There are several reports demonstrating the correlation between natriuresis and diuresis and plasma ANP levels in response to systemic volume expansion, e.g., atrial balloon inflation, blood volume expansion, salt load, and water immersion (4,7,17,32,50,59). These responses depend on the activation of sinoaortic baroreceptors and/or cardiopulmonary receptor afferents located in the atria, lungs, great veins, and ventricles that project to the nucleus of the solitary tract (NTS) (1, 12, 22). The NTS neurons convey blood volume expansion signals and project to and excite different areas within the forebrain and hindbrain to produce neuroendocrine responses. Studies using expression of the immediate early gene c-Fos as a marker of neuronal activation have shown that, in addition to the NTS, volume-loading activates the paraventricular (PVN) and supraoptic (SON) nuclei, dorsal raphe nucleus (DRN), caudal ventrolateral medulla, locus coeruleus, and also the lateral parabrachial nucleus (LPBN) (6,20,46). The LPBN, a structure lying dorsolateral to the superior cerebellar peduncle, has been shown to play an ...

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“…Although the precise function of the hindbrain in control of dipsogenic behavior is not clear, systemic hyperosmolality induces c-fos expression in the adult AP, NTS, and LPBN (32), suggesting a role in the control of body fluid homeostasis. In rats, lesions of the AP and the adjacent caudal NTS, or destruction of bilateral LPBN, to which the AP and NTS have substantial secondary projections, results in large increases in water and salt intake in response to angiotensin II, compared with control animals (25,(33)(34)(35). From these observations, it has been hypothesized that AP-NTS-LBPN systems comprise inhibitory mechanisms for dipsogenic responses.…”

Section: Discussionmentioning

confidence: 99%

Plasma Osmolality Dipsogenic Thresholds and c-fos Expression in the Near-Term Ovine Fetus

Nijland

Ross

2001

Pediatr Res

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In ovine and human pregnancy, fetal swallowing contributes importantly to amniotic fluid homeostasis. Fetal dipsogenic responsiveness to short-term plasma hyperosmolality develops in late gestation, although fetal swallowing is not stimulated in response to long-term plasma osmolality increases (2 to 3%), which typically stimulate adult drinking behavior. To explore the near-term fetal plasma osmolality threshold for swallowing stimulation, we examined the effects of i.v. hypertonic saline-induced subacute increases in plasma hypertonicity on fetal swallowing behavior. Central sites of activation were examined by c-fos expression in putative dipsogenic nuclei. The results demonstrate that subacute 2 to 3% plasma osmolality increases do not stimulate near-term ovine fetal swallowing. However, fetal swallowing activity significantly increased (3 times) after plasma osmolality increased Ͼ6% above basal values. Consistent with a specific dipsogenic response, i.v. hypertonic saline induced c-fos expression in the anterior third ventricle region, a putative dipsogenic center, as well as in the fetal hindbrain. The stimulation of fetal swallowing under conditions of higher osmotic stimulation and the correlation with forebrain c-fos expression indicates that near-term fetal osmoregulation mechanisms are functional, although not completely mature. Intravascular osmolality and body fluid homeostasis are maintained primarily by coordination of thirst-mediated drinking behavior and neuroendocrine-mediated renal fluid regulatory mechanisms. During in utero development, fetal swallowing contributes importantly to amniotic fluid volume homeostasis. Previous studies in this laboratory have demonstrated that near-term ovine fetal swallowing is stimulated by intravenous, intracarotid, and intracerebroventricular hyperosmolality (1-4), consistent with the activation of central osmoreceptors in regions responsive to both vascular and cerebrospinal fluid tonicity. Despite intact fetal osmotic-dipsogenic responsiveness, fetal swallowing is not stimulated in response to plasma osmolality increases (2 to 3%), which typically stimulate adult drinking behavior. For example, despite continually elevated plasma osmolality (10 -14 mosmol/kg) in response to short-term i.v. hypertonic saline injection, fetal swallowing activity is only stimulated for a maximum of 5 min (1). Furthermore, long-term increases in plasma osmolality of 10 mosmol/kg do not alter fetal swallowed volume (5). These responses suggest either a reduced population of fetal osmoreceptor cells, reduced sensitivity of osmoreceptors, or altered secondary neural mechanisms, in comparison to the adult. c-fos expression has been well described as a marker of neuronal activation in both adult and fetal brain nuclei (6). McDonald et al. (7) recently showed that FOS-ir was evident in the SFO, OVLT, and MnPO, as well as in the PVN and SON of the near-term fetal forebrain in response to maternal hypertonicity. These results are comparable to physiological and c-fos responses observe...

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Lesions in lateral parabrachial nucleus enhance drinking to angiotensin II and isoproterenol

Cited by 53 publications

References 0 publications

Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

Plasma Osmolality Dipsogenic Thresholds and c-fos Expression in the Near-Term Ovine Fetus

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