Experimental Gestational Diabetes Mellitus Induces Blunted Vasoconstriction and Functional Changes in the Rat Aorta

Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular...

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Published in:	BioMed research international Vol. 2014; no. 2014; pp. 1 - 11
Main Authors:	Bracho-Valdés, Ismael, Ibarra-Barajas, Maximiliano, Villanueva, Cleva, Tufiño, Cecilia, Bobadilla-Lugo, Rosa Amalia
Format:	Journal Article
Language:	English
Published:	Cairo, Egypt Hindawi Publishing Corporation 01-01-2014 John Wiley & Sons, Inc Hindawi Limited
Subjects:	Angiotensin II - administration & dosage Animals Aorta Diabetes in pregnancy Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - physiopathology Diabetes, Gestational - chemically induced Diabetes, Gestational - drug therapy Diabetes, Gestational - physiopathology Female Glucose Humans Insulin Insulin resistance Losartan - administration & dosage Obesity Phenylephrine - administration & dosage Physiological aspects Pregnancy Rats Rodents Vasoconstriction Vasoconstriction - drug effects Vasoconstrictor Agents - administration & dosage Vasodilation - drug effects
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Abstract	Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT1R, AT2R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response ( P < 0.05 versus SD) in intact (e+) but not in endothelium-free (e−) vessels. Losartan reduced GDM but not SD e− vasoconstriction ( P < 0.01 versus SD). AT1R, AT2R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels ( P < 0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT2 vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations.
AbstractList	Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT1R, AT2R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response ( P < 0.05 versus SD) in intact (e+) but not in endothelium-free (e−) vessels. Losartan reduced GDM but not SD e− vasoconstriction ( P < 0.01 versus SD). AT1R, AT2R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels ( P < 0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT2 vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations. Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT1R, AT2R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response ( P < 0.05 versus SD) in intact (e+) but not in endothelium-free (e-) vessels. Losartan reduced GDM but not SD e- vasoconstriction ( P < 0.01 versus SD). AT1R, AT2R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels ( P < 0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT2 vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations. Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT1R, AT2R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response (P < 0.05 versus SD) in intact (e+) but not in endothelium-free (e-) vessels. Losartan reduced GDM but not SD e- vasoconstriction (P < 0.01 versus SD). AT1R, AT2R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels (P < 0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT2 vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations. Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT sub(1) R, AT sub(2) R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response (P<0.05 versus SD) in intact (e+) but not in endothelium-free (e-) vessels. Losartan reduced GDM but not SD e- vasoconstriction (P<0.01 versus SD). AT sub(1) R, AT sub(2) R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels (P<0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT sub(2) vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations. Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT 1 R, AT 2 R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response ( P < 0.05 versus SD) in intact (e+) but not in endothelium-free (e−) vessels. Losartan reduced GDM but not SD e− vasoconstriction ( P < 0.01 versus SD). AT 1 R, AT 2 R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels ( P < 0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT 2 vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations. Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric diet (HD) induced gestational diabetes mellitus (GDM), so the objective of this work was to determine the effects of HD induced GDM on vascular responses. Angiotensin II as well as phenylephrine induced vascular contraction was tested in isolated aorta rings with and without endothelium from rats fed for 7 weeks (4 before and 3 weeks during pregnancy) with standard (SD) or hypercaloric (HD) diet. Also, protein expression of AT 1 R, AT 2 R, COX-1, COX-2, NOS-1, and NOS-3 and plasma glucose, insulin, and angiotensin II levels were measured. GDM impaired vasoconstrictor response ( P < 0.05 versus SD) in intact (e+) but not in endothelium-free (e−) vessels. Losartan reduced GDM but not SD e− vasoconstriction ( P < 0.01 versus SD). AT 1 R, AT 2 R, and COX-1 and COX-2 protein expression were significantly increased in GDM vessels ( P < 0.05 versus SD). Results suggest an increased participation of endothelium vasodilator mediators, probably prostaglandins, as well as of AT 2 vasodilator receptors as a compensatory mechanism for vasoconstrictor changes generated by experimental GDM. Considering the short term of rat pregnancy findings can reflect early stage GDM adaptations.
Audience	Academic
Author	Bracho-Valdés, Ismael Bobadilla-Lugo, Rosa Amalia Villanueva, Cleva Ibarra-Barajas, Maximiliano Tufiño, Cecilia
AuthorAffiliation	2 Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Avenida De los Barrios 1, Los Reyes Iztacala, 54090 Tlalnepantla, Mexico 1 Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Santo Tomás, 11340 DF, Mexico
AuthorAffiliation_xml	– name: 1 Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Santo Tomás, 11340 DF, Mexico – name: 2 Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Avenida De los Barrios 1, Los Reyes Iztacala, 54090 Tlalnepantla, Mexico
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/25610861$$D View this record in MEDLINE/PubMed
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CitedBy_id	crossref_primary_10_1002_ar_23510 crossref_primary_10_3109_10641963_2015_1060984 crossref_primary_10_1016_j_preghy_2024_01_131
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Copyright	Copyright © 2014 Cecilia Tufiño et al. COPYRIGHT 2015 John Wiley & Sons, Inc. Copyright © 2014 Cecilia Tufiño et al. Cecilia Tufiño et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2014 Cecilia Tufiño et al. 2014
Copyright_xml	– notice: Copyright © 2014 Cecilia Tufiño et al. – notice: COPYRIGHT 2015 John Wiley & Sons, Inc. – notice: Copyright © 2014 Cecilia Tufiño et al. Cecilia Tufiño et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright © 2014 Cecilia Tufiño et al. 2014
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10.1161/01.res.0000056759.53828.2c
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Snippet	Diabetic conditions increase vascular reactivity to angiotensin II in several studies but there are scarce reports on cardiovascular effects of hypercaloric...
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SubjectTerms	Angiotensin II - administration & dosage Animals Aorta Diabetes in pregnancy Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - physiopathology Diabetes, Gestational - chemically induced Diabetes, Gestational - drug therapy Diabetes, Gestational - physiopathology Female Glucose Humans Insulin Insulin resistance Losartan - administration & dosage Obesity Phenylephrine - administration & dosage Physiological aspects Pregnancy Rats Rodents Vasoconstriction Vasoconstriction - drug effects Vasoconstrictor Agents - administration & dosage Vasodilation - drug effects
Title	Experimental Gestational Diabetes Mellitus Induces Blunted Vasoconstriction and Functional Changes in the Rat Aorta
URI	https://search.emarefa.net/detail/BIM-1034434 https://dx.doi.org/10.1155/2014/329634 https://www.ncbi.nlm.nih.gov/pubmed/25610861 https://www.proquest.com/docview/1644409904 https://search.proquest.com/docview/1652392538 https://search.proquest.com/docview/1660394099 https://pubmed.ncbi.nlm.nih.gov/PMC4291015
Volume	2014
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