Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin-angiotensin system (2008)
- Authors:
- USP affiliated authors: FURUKAWA, LUZIA NAOKO SHINOHARA - FM ; HEIMANN, JOEL CLAUDIO - FM ; SHIMIZU, MARIA HELOISA MASSOLA - FM
- Unidade: FM
- DOI: 10.1016/j.physbeh.2008.05.011
- Subjects: GRAVIDEZ (DIETOTERAPIA); CIRCULAÇÃO FETAL; PRESSÃO SANGUÍNEA
- Language: Inglês
- Imprenta:
- Source:
- Título: Physiology & Behavior
- ISSN: 0031-9384
- Volume/Número/Paginação/Ano: v. 95, n. 1-2, p. 145-151, 2008
- Este periódico é de acesso aberto
- Este artigo NÃO é de acesso aberto
-
ABNT
LEANDRO, Sandra Márcia et al. Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin-angiotensin system. Physiology & Behavior, v. 95, n. 1-2, p. 145-151, 2008Tradução . . Disponível em: https://doi.org/10.1016/j.physbeh.2008.05.011. Acesso em: 11 fev. 2026. -
APA
Leandro, S. M., Furukawa, L. N. S., Shimizu, M. H. M., Casarini, D. E., Seguro, A. C., Patriarca, G., et al. (2008). Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin-angiotensin system. Physiology & Behavior, 95( 1-2), 145-151. doi:10.1016/j.physbeh.2008.05.011 -
NLM
Leandro SM, Furukawa LNS, Shimizu MHM, Casarini DE, Seguro AC, Patriarca G, Araújo MSC, Dolnikoff MS, Heimann JC. Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin-angiotensin system [Internet]. Physiology & Behavior. 2008 ; 95( 1-2): 145-151.[citado 2026 fev. 11 ] Available from: https://doi.org/10.1016/j.physbeh.2008.05.011 -
Vancouver
Leandro SM, Furukawa LNS, Shimizu MHM, Casarini DE, Seguro AC, Patriarca G, Araújo MSC, Dolnikoff MS, Heimann JC. Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin-angiotensin system [Internet]. Physiology & Behavior. 2008 ; 95( 1-2): 145-151.[citado 2026 fev. 11 ] Available from: https://doi.org/10.1016/j.physbeh.2008.05.011 - High-Salt Intake Induces Cardiomyocyte Hypertrophy in Rats in Response to Local Angiotensin II Type 1 Receptor Activation1–3
- N-acetyl-L-cysteine exacerbates kidney dysfunction caused by a chronic high-sodium diet in renal ischemia and reperfusion rats
- Maternal renin-angiotensin system (RAS) blockade: Effect on adult offspring
- Sucrose overload during pregnancy and lactation influences blood presure, body weight, and adipose tissue mass in adult offspring
- Myocardial hypertrophy induced by high salt consumption is prevented by angiotensin II AT2 receptor agonist
- Body weight is influenced by the degree of salt intake and this association is due to changes in energy balance and hormonal profile
- Low salt intake modulates tissue insulin signaling, JNK activity and IRS-1ser307 phosphorylation
- Effect of salt intake on the placental angiotensin-converting enzyme activity (ACE) during pregnancy
- Differential sympathetic and angiotensinergic responses in rats submitted to low- or high-salt diet
- Salt overload during pregnancy alters uterine blood flow, placenta renin angiotensin system (RAS) and placenta weight
Informações sobre o DOI: 10.1016/j.physbeh.2008.05.011 (Fonte: oaDOI API)
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
