Terezila Machado Coimbra

Universidade de São Paulo

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José Antunes‐Rodrigues

Universidade de São Paulo

Heloı́sa Della Coletta Francescato

Universidade de São Paulo

Cleonice Giovanini Alves da Silva

Universidade de São Paulo

Luiz G.S. Branco

Universidade de São Paulo

Roberto Silva Costa

Universidade de São Paulo

Lucas Ferreira de Almeida

University of Virginia

Jonatas E. Nogueira

Universidade de Fortaleza

Gilberto De Nucci

Universidade Estadual de Campinas (UNICAMP)

A L Favaretto

Universidade de São Paulo

Antônio Roberto Martins

Yale University

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Universidade de São Paulo

Universidade de Ribeirão Preto

Clinics Hospital of Ribeirão Preto

Universidade Brasil

Universidade Estadual Paulista (Unesp)

Universidade de Fortaleza

Universidade Estadual de Campinas (UNICAMP)

Hospital Universitário da Universidade de São Paulo

Université de Montréal

Universidade Federal da Bahia

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Effect of Physical Exercise on the Febrigenic Signaling is Modulated by Preoptic Hydrogen Sulfide Production

PLoS ONE (2017)

Jonatas E. Nogueira Renato Nery Soriano Rodrigo Alberto Restrepo Fernández Heloísa D. C. Francescato Rafael Simone Saia

We tested the hypothesis that the neuromodulator hydrogen sulfide (H2S) in the preoptic area (POA) of the hypothalamus modulates the febrigenic signaling differently in sedentary and trained rats. Besides H2S production rate and protein expressions of H2S-related synthases cystathionine β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MPST) and cystathionine γ-lyase (CSE) in the POA, we also measured deep body temperature (Tb), circulating plasma levels of cytokines and corticosterone in an animal model of systemic inflammation. Rats run on a treadmill before receiving an intraperitoneal injection of lipopolysaccharide (LPS, 100 μg/kg) or saline. The magnitude of changes of Tb during the LPS-induced fever was found to be similar between sedentary and trained rats. In sedentary rats, H2S production was not affected by LPS. Conversely, in trained rats LPS caused a sharp increase in H2S production rate that was accompanied by an increased CBS expression profile, whereas 3-MPST and CSE expressions were kept relatively constant. Sedentary rats showed a significant LPS-induced release of cytokines (IL-1β, IL-6, and TNF-α) which was virtually abolished in the trained animals. Correlation between POA H2S and IL-6 as well as TNF-α was observed. Corticosterone levels were augmented after LPS injection in both groups. We found correlations between H2S and corticosterone, and corticosterone and IL-1β. These data are consistent with the notion that the responses to systemic inflammation are tightly regulated through adjustments in POA H2S production which may play an anti-inflammatory role downmodulating plasma cytokines levels and upregulating corticosterone release.

Corticosterone

Preoptic area

Proinflammatory cytokine

Intraperitoneal injection

Cystathionine gamma-lyase

10.1371/journal.pone.0170468

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Atrial natriuretic peptide and oxytocin induce natriuresis by release of cGMP

Proceedings of the National Academy of Sciences (1999)

Telma de Jesus Soares Terezila Machado Coimbra Antônio Roberto Martins Athayde Pereira Evelin Capellari Cárnio

Our hypothesis is that oxytocin (OT) causes natriuresis by activation of renal NO synthase that releases NO followed by cGMP that mediates the natriuresis. To test this hypothesis, an inhibitor of NO synthase, l -nitroarginine methyl ester (NAME), was injected into male rats. Blockade of NO release by NAME had no effect on natriuresis induced by atrial natriuretic peptide (ANP). This natriuresis presumably is caused by cGMP because ANP also activates guanylyl cyclase, which synthesizes cGMP from GTP. The 18-fold increase in sodium (Na + ) excretion induced by OT (1 μg) was accompanied by an increase in urinary cGMP and preceded by 20 min a 20-fold increase in NO 3 − excretion. NAME almost completely inhibited OT-induced natriuresis and increased NO 3 − excretion; however, when the dose of OT was increased 10-fold, a dose that markedly increases plasma ANP concentrations, NAME only partly inhibited the natriuresis. We conclude that the natriuretic action of OT is caused by a dual action: generation of NO leading to increased cGMP and at higher doses release of ANP that also releases cGMP. OT-induced natriuresis is caused mainly by decreased tubular Na + reabsorption mediated by cGMP. In contrast to ANP that releases cGMP in the renal vessels and the tubules, OT acts on its receptors on NOergic cells demonstrated in the macula densa and proximal tubules to release cGMP that closes Na + channels. Both ANP- and OT-induced kaliuresis also appear to be mediated by cGMP. We conclude that cGMP mediates natriuresis and kaliuresis induced by both ANP and OT.

Kaliuresis

Atrial natriuretic peptide

Macula densa

10.1073/pnas.96.1.278

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Protective effect of calcitriol on rhabdomyolysis-induced acute kidney injury in rats

Scientific Reports (2019)

Natany Garcia Reis Heloı́sa Della Coletta Francescato Lucas Ferreira de Almeida Cleonice Giovanini Alves da Silva Roberto Silva Costa

Abstract Glycerol injection in rats can lead to rhabdomyolysis, with the release of the intracellular muscle content to the extracellular compartment and acute kidney injury (AKI). Oxidative stress and the inflammatory processes contribute to the disturbances in renal function and structure observed in this model. This study evaluated the effect of calcitriol administration in AKI induced by rhabdomyolysis and its relationship with oxidative damage and inflammatory process. Male Wistar Hannover rats were treated with calcitriol (6 ng/day) or vehicle (0.9% NaCl) for 7 days and were injected with 50% glycerol or saline 3 days after the beginning of calcitriol or saline administration. Four days after glycerol or saline injection, urine, plasma and renal tissue samples were collected for renal function and structural analysis. The oxidative stress and the inflammatory processes were also evaluated. Glycerol-injected rats presented increased sodium fractional excretion and decreased glomerular filtration rates. These alterations were associated with tubular injury in the renal cortex. These animals also presented increased oxidative damage, apoptosis, inflammation, higher urinary excretion of vitamin D-binding protein and decreased cubilin expression in renal tissue. All these alterations were less intense in calcitriol-treated animals. This effect was associated with decreases in oxidative damage and inflammation.

10.1038/s41598-019-43564-1

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Calcitriol reduces kidney development disorders in rats provoked by losartan administration during lactation

Scientific Reports (2017)

Lucas Ferreira de Almeida Heloı́sa Della Coletta Francescato Cleonice Giovanini Alves da Silva Roberto Silva Costa Terezila Machado Coimbra

Calcitriol has important effects on cellular differentiation and proliferation, as well as on the regulation of the renin gene. Disturbances in renal development can be observed in rats exposed to angiotensin II (AngII) antagonists during lactation period. The lack of tubular differentiation in losartan-treated rats can affect calcitriol uptake. This study evaluated the effect of calcitriol administration in renal development disturbances in rats provoked by losartan (AngII type 1 receptor antagonist) administration during lactation. Animals exposed to losartan presented higher albuminuria, systolic blood pressure, increased sodium and potassium fractional excretion, and decreased glomerular filtration rate compared to controls. These animals also showed a decreased glomerular area and a higher interstitial relative area from the renal cortex, with increased expression of fibronectin, alpha-SM-actin, vimentin, and p-JNK; and an increased number of macrophages, p-p38, PCNA and decreased cubilin expression. Increased urinary excretion of MCP-1 and TGF-β was also observed. All these alterations were less intense in the losartan + calcitriol group.The animals treated with calcitriol showed an improvement in cellular differentiation, and in renal function and structure. This effect was associated with reduction of cell proliferation and inflammation.

10.1038/s41598-017-11815-8

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Citations (16)