Experimental gestational diabetes mellitus induces blunted vasoconstriction and functional changes in the rat aorta.

Cecilia Tufiño, Cleva Villanueva-López, Maximiliano Ibarra-Barajas, Ismael Bracho-Valdés, Rosa Amalia Bobadilla-Lugo
Author Information
  1. Cecilia Tufiño: 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.
  2. Cleva Villanueva-López: 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.
  3. Maximiliano Ibarra-Barajas: Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Avenida De los Barrios 1, Los Reyes Iztacala, 54090 Tlalnepantla, Mexico.
  4. Ismael Bracho-Valdés: 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.
  5. Rosa Amalia Bobadilla-Lugo: 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.

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.

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MeSH Term

Angiotensin II
Animals
Diabetes Mellitus, Experimental
Diabetes, Gestational
Female
Humans
Losartan
Phenylephrine
Pregnancy
Rats
Vasoconstriction
Vasoconstrictor Agents
Vasodilation

Chemicals

Vasoconstrictor Agents
Angiotensin II
Phenylephrine
Losartan

Word Cloud

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