Whole body sodium depletion modifies <scp>AT</scp>1 <scp>mRNA</scp> expression and serotonin content in the dorsal raphe nucleus

Porcari, C.Y.; Araujo, Iracema; Urzedo-Rodrigues, Lilia S.; Luca, Laurival A. De; Menani, José Vanderlei; Caeiro, Ximena E.; Imboden, Hans; Antunes‐Rodrigues, José; Reis, L. C.; Vivas, Laura; Godino, Andrea; Mecawi, André Souza

doi:10.1111/jne.12703

Cited by 14 publications

(17 citation statements)

References 45 publications

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“…In this protocol, rats have free access to a low sodium diet and distilled water for 24 h after acute furosemide treatment, allowing them to reestablish, at least in part, the water lost but not the sodium. This results in the development of hyponatremia and hypoosmolality and consequently inhibition of water intake as demonstrated before [7,9,26] and in 24 h measurements in the present study. Despite modulating thirst, changes as small as 1-2% in ECF osmolality are able to modulate neurohypophysial hormones secretion, whereas changes of 8-15% in ECF volume are required to produce a similar effect.…”

Section: Discussionsupporting

confidence: 79%

“…The loop diuretic furosemide is used to induce sodium excretion and ECF volume depletion by blocking the cotransporter NKCC2 in the thick ascending limb of the loop of Henle. This approach is widely used to study the control of hydromineral balance in the hyponatremic/hypovolemic context [6][7][8][9] and for the treatment of hypertension, oedematous disorders and the management of hypervolemia and electrolyte disorders [5]. However, the physiological and molecular consequences of 24 h of body sodium and ECF volume depletion with furosemide on the HNS were not well known.…”

Section: Discussionmentioning

confidence: 99%

“…NKCC2 cotransporter blockade also decreases medullary hypertonicity and the osmotic driving force for water reabsorption, resulting in an isosmotic ECF volume loss [6,7]. As a consequence of body sodium and ECF volume loss, the renin-angiotensin-aldosterone system (RAAS) and sodium appetite are activated [7][8][9]. Recently, experiments performed in transgenic rats expressing green fluorescent protein under the AVP promoter demonstrated that a single administration of furosemide acutely increased Fos-like immunoreactivity and AVP expression in the SON and in magnocellular PVN neurons [10].…”

Section: Introductionmentioning

confidence: 99%

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Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

Dutra¹,

Paterson²,

Monteiro³

et al. 2020

Neuroendocrinology

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Background/Aims: Furosemide is a loop diuretic widely used in clinical practice for the treatment of oedema and hypertension. The aim of this study was to determine physiological and molecular changes in the hypothalamic-neurohypophysial system as a consequence of furosemide-induced sodium depletion. Methods: Male rats were sodium depleted by acute furosemide injection (10 and 30 mg/kg) followed by access to low sodium diet and distilled water for 24 h. The renal and behavioural consequences were evaluated, while blood and brains were collected to evaluate the neuroendocrine and gene expression responses. Results: Furosemide treatment acutely increases urinary sodium and water excretion. After 24 h, water and food intake were reduced, while plasma angiotensin II and corticosterone were increased. After hypertonic saline presentation, sodium-depleted rats showed higher preference for salt. Interrogation using RNA sequencing revealed the expression of 94 genes significantly altered in the hypothalamic paraventricular nucleus (PVN) of sodium-depleted rats (31 upregulated and 63 downregulated). Out of 9 genes chosen, 5 were validated by quantitative PCR in the PVN (upregulated: Ephx2, Ndnf and Vwf; downregulated: Caprin2 and Opn3). The same genes were also assessed in the supraoptic nucleus (SON, upregulated: Tnnt1, Mis18a, Nr1d1 and Dbp; downregulated: Caprin2 and Opn3). As a result of these plastic transcriptome changes, vasopressin expression was decreased in PVN and SON, whilst vasopressin and oxytocin levels were reduced in plasma. Conclusions: We thus have identified novel genes that might regulate vasopressin gene expression in the hypothalamus controlling the magnocellular neurons secretory response to body sodium depletion and consequently hypotonic stress.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

Dutra¹,

Paterson²,

Monteiro³

et al. 2020

Neuroendocrinology

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“…), after which the rats were given free access to low‐Na + diet (powdered corn meal, 0.001% Na + ) and distilled water for 24 h, as described by Porcari et al. (). At 2 and 24 h after frusemide injection, urine was collected to evaluate urinary volume and Na + excretion.…”

Section: Methodsmentioning

confidence: 99%

“…After OVX, control animals received corn oil (OVX, n = 12) or oestradiol treatment (OVX+E 2 , n = 12) and spontaneous water, food and 0.3 M NaCl intake and urinary parameters were evaluated daily for 7 days. On the seventh day, the hypertonic saline bottle were removed and the rats were submitted to wholebody Na + depletion induced by frusemide (Lasix; Suzano, SP, Brazil, 20 mg kg −1 ; S.C.), after which the rats were given free access to low-Na + diet (powdered corn meal, 0.001% Na + ) and distilled water for 24 h, as described by Porcari et al (2019). At 2 and 24 h after frusemide injection, urine was collected to evaluate urinary volume and Na + excretion.…”

Section: Ovariectomy and Oestrogen Replacementmentioning

confidence: 99%

Acute body sodium depletion induces skin sodium mobilization in female Wistar rats

Lopes‐Menezes

Dos‐Santos

Felintro

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Can Na+ depletion mobilize Na+ from the skin reservoir in ovariectomized rats? Does oestrogen replacement change the amount and the dynamics of skin Na+ storage? Is the reduced salt appetite after Na+ depletion in ovariectomized rats with oestrogen replacement related to changes in the skin Na+? What is the main finding and its importance?This work demonstrated that acute body Na+ depletion induced by frusemide mobilized the osmotically inactive skin Na+ reservoir to become osmotically active. Oestrogen treatment decreased the induced Na+ intake in ovariectomized rats but did not modulate the inactive Na+ reservoir in control conditions or its mobilization induced by Na+ depletion. Abstract Oestradiol, which is an important hormone for water and electrolyte balance, also has a role in the inhibition of induced Na+ appetite. Sodium can be stored in the skin in osmotically active or inactive forms, and this skin Na+ reservoir may be involved in the control of body Na+ levels during physiopathological challenges. In this study, we investigated whether the effect of sodium depletion by frusemide can mobilize Na+ from the skin reservoir and whether oestradiol replacement changes or mobilizes the Na+ reserves in the skin. Ovariectomized Wistar rats were treated with vehicle or oestradiol for 7 days to evaluate the effects of oestrogen on the hydroelectrolyte balance, intake responses and skin Na+ and water content in basal conditions. Furthermore, the effects of oestrogen were evaluated after 24 h frusemide‐induced whole‐body Na+ depletion. Oestradiol‐replaced rats exhibited reduced water intake without any significant changes in salt intake, Na+ excretion or water and Na+ skin content in basal conditions. After sodium depletion, both vehicle‐ and oestradiol‐treated rats exhibited an increase in the osmotically active skin Na+, which was associated with a decrease of the inactive skin Na+ reservoir. Oestrogen decreased the hypertonic saline intake induced by Na+ depletion, but it was not associated with any significant changes in the skin Na+ reservoir. Thus, sodium depletion is able to change the inactive–active skin Na+ reservoir balance. However, the oestrogenic modulation of sodium appetite after Na+ depletion is probably not related to the action of this hormone in the skin Na+ reservoir balance.

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Aconitine disrupts serotonin neurotransmission via 5‐hydroxytryptamine receptor in zebrafish embryo

Chen

Wang

et al. 2020

J of Applied Toxicology

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Medicinal plants of the genus Aconitum are one of the most commonly used herbs in traditional medicine in East Asia to treat conditions related to the heart, pain, or inflammation. However, these herbs are also dangerous as accidental poisoning due to misuse is a recurring issue. These plants contain a number of diester‐diterpenoid alkaloid compounds and aconitine is the most abundant and active one. This study investigated neurotoxicity of aconitine to zebrafish embryos in early development in relation to serotonin regulation. Experimental results showed that aconitine exposure (1, 10, and 100 μM) increased frequency of coiling behavior in zebrafish embryos in a dose‐dependent manner and this effect can be triggered by either exposure to 5‐hydroxytryptamine 1A (5‐HT1A) receptor agonist (±)‐8‐hydroxy‐2‐(dipropylamino)tetralin (8‐OH‐DPAT) or overexpression of serotonin receptor 5‐htr1ab. At the same time, coiling behavior caused by aconitine exposure could be rescued by co‐exposure to 5‐HT1A receptor antagonist WAY‐100635 Maleate (WAY100635) and knockdown of 5‐htr1ab using morpholino. Exposure to aconitine also significantly increased serotonin receptor 5‐htr1ab and 5‐htr1bd gene expression at 24 h post fertilization (hpf), but decreased their expression and protein expression of the serotonin receptor at 96 hpf with the high dose. These results suggest that neurotoxicity caused by aconitine is mediated through the 5‐HT receptor.

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Whole body sodium depletion modifies AT1 mRNA expression and serotonin content in the dorsal raphe nucleus

Cited by 14 publications

References 45 publications

Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

Acute body sodium depletion induces skin sodium mobilization in female Wistar rats

Aconitine disrupts serotonin neurotransmission via 5‐hydroxytryptamine receptor in zebrafish embryo

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