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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.
Physiol Behav. 2008 Sep 03; 95(1-2):145-51.PB

Abstract

A number of studies conducted in humans and in animals have observed that events occurring early in life are associated with the development of diseases in adulthood. Salt overload and restriction during pregnancy and lactation are responsible for functional (hemodynamic and hormonal) and structural alterations in adult offspring. Our group observed that lower birth weight and insulin resistance in adulthood is associated with salt restriction during pregnancy. On the other hand, perinatal salt overload is associated with higher blood pressure and higher renal angiotensin II content in adult offspring. Therefore, we hypothesised that renin-angiotensin system (RAS) function is altered by changes in sodium intake during pregnancy. Such changes may influence fetoplacental blood flow and thereby fetal nutrient supply, with effects on growth in utero and, consequently, on birth weight. Female Wistar rats were fed low-salt (LS), normal-salt (NS), or high-salt (HS) diet, starting before conception and continuing until day 19 of pregnancy. Blood pressure, heart rate, fetuses and dams' body weight, placentae weight and litter size were measured on day 19 of pregnancy. Cardiac output, uterine and placental blood flow were also determined on day 19. Expressions of renin-angiotensin system components and of the TNF-alpha gene were evaluated in the placentae. Plasma renin activity (PRA) and plasma and tissue angiotensin-converting enzyme (ACE) activity, as well as plasma and placental levels of angiotensins I, II, and 1-7 were measured. Body weight and kidney mass were greater in HS than in NS and LS dams. Food intake did not differ among the maternal groups. Placental weight was lower in LS dams than in NS and HS dams. Fetal weight was lower in the LS group than in the NS and HS groups. The PRA was greater in LS dams than in NS and HS dams, although ACE activity (serum, cardiac, renal, and placental) was unaffected by the level of sodium intake. Placental levels of angiotensins I and II were lower in the HS group than in the NS and LS groups. Placental angiotensin receptor type 1 (AT(1)) gene expression and levels of thiobarbituric acid reactive substances (TBARS) were higher in HS dams, as were uterine blood flow and cardiac output. The degree of salt intake did not influence plasma sodium, potassium or creatinine. Although fractional sodium excretion was higher in HS dams than in NS and LS dams, fractional potassium excretion was unchanged. In conclusion, findings from this study indicate that the reduction in fetal weight in response to salt restriction during pregnancy does not involve alterations in uterine-placental perfusion or the RAS. Moreover, no change in fetal weight is observed in response to salt overload during pregnancy. However, salt overload did lead to an increase in placental weight and uterine blood flow associated with alterations in maternal plasma and placental RAS. Therefore, these findings indicate that changes in salt intake during pregnancy lead to alterations in uterine-placental perfusion and fetal growth.

Authors+Show Affiliations

Department of Internal Medicine, Laboratory of Experimental Hypertension, University of São Paulo School of Medicine, São Paulo, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18572207

Citation

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, vol. 95, no. 1-2, 2008, pp. 145-51.
Leandro SM, Furukawa LN, Shimizu MH, 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. Physiol Behav. 2008;95(1-2):145-51.
Leandro, S. M., Furukawa, L. N., Shimizu, M. H., Casarini, D. E., Seguro, A. C., Patriarca, G., Coelho, M. S., Dolnikoff, M. S., & Heimann, J. C. (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), 145-51. https://doi.org/10.1016/j.physbeh.2008.05.011
Leandro SM, 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. Physiol Behav. 2008 Sep 3;95(1-2):145-51. PubMed PMID: 18572207.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Leandro,Sandra Márcia, AU - Furukawa,Luzia Naôko Shinohara, AU - Shimizu,Maria Heloisa Massola, AU - Casarini,Dulce Elena, AU - Seguro,Antonio Carlos, AU - Patriarca,Giuliana, AU - Coelho,Michella Soares, AU - Dolnikoff,Miriam Sterman, AU - Heimann,Joel Claudio, Y1 - 2008/05/21/ PY - 2007/08/27/received PY - 2008/05/12/revised PY - 2008/05/13/accepted PY - 2008/6/24/pubmed PY - 2008/12/19/medline PY - 2008/6/24/entrez SP - 145 EP - 51 JF - Physiology & behavior JO - Physiol. Behav. VL - 95 IS - 1-2 N2 - A number of studies conducted in humans and in animals have observed that events occurring early in life are associated with the development of diseases in adulthood. Salt overload and restriction during pregnancy and lactation are responsible for functional (hemodynamic and hormonal) and structural alterations in adult offspring. Our group observed that lower birth weight and insulin resistance in adulthood is associated with salt restriction during pregnancy. On the other hand, perinatal salt overload is associated with higher blood pressure and higher renal angiotensin II content in adult offspring. Therefore, we hypothesised that renin-angiotensin system (RAS) function is altered by changes in sodium intake during pregnancy. Such changes may influence fetoplacental blood flow and thereby fetal nutrient supply, with effects on growth in utero and, consequently, on birth weight. Female Wistar rats were fed low-salt (LS), normal-salt (NS), or high-salt (HS) diet, starting before conception and continuing until day 19 of pregnancy. Blood pressure, heart rate, fetuses and dams' body weight, placentae weight and litter size were measured on day 19 of pregnancy. Cardiac output, uterine and placental blood flow were also determined on day 19. Expressions of renin-angiotensin system components and of the TNF-alpha gene were evaluated in the placentae. Plasma renin activity (PRA) and plasma and tissue angiotensin-converting enzyme (ACE) activity, as well as plasma and placental levels of angiotensins I, II, and 1-7 were measured. Body weight and kidney mass were greater in HS than in NS and LS dams. Food intake did not differ among the maternal groups. Placental weight was lower in LS dams than in NS and HS dams. Fetal weight was lower in the LS group than in the NS and HS groups. The PRA was greater in LS dams than in NS and HS dams, although ACE activity (serum, cardiac, renal, and placental) was unaffected by the level of sodium intake. Placental levels of angiotensins I and II were lower in the HS group than in the NS and LS groups. Placental angiotensin receptor type 1 (AT(1)) gene expression and levels of thiobarbituric acid reactive substances (TBARS) were higher in HS dams, as were uterine blood flow and cardiac output. The degree of salt intake did not influence plasma sodium, potassium or creatinine. Although fractional sodium excretion was higher in HS dams than in NS and LS dams, fractional potassium excretion was unchanged. In conclusion, findings from this study indicate that the reduction in fetal weight in response to salt restriction during pregnancy does not involve alterations in uterine-placental perfusion or the RAS. Moreover, no change in fetal weight is observed in response to salt overload during pregnancy. However, salt overload did lead to an increase in placental weight and uterine blood flow associated with alterations in maternal plasma and placental RAS. Therefore, these findings indicate that changes in salt intake during pregnancy lead to alterations in uterine-placental perfusion and fetal growth. SN - 0031-9384 UR - https://www.unboundmedicine.com/medline/citation/18572207/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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0031-9384(08)00159-5 DB - PRIME DP - Unbound Medicine ER -