Changes in vascular reactivity of the coronary artery and thoracic aorta in the delta sarcoglycan null mutant mice

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Abstract

© 2017, Iranian Society of Physiology and Pharmacology. All rights reserved. Introduction: Mutations in the delta sarcoglycan gene (d-SG) cause limb-girdle muscular dystrophy type 2F with structural and functional alterations in cardiac, smooth and skeletal muscle. The objective of the present study was to improve information about changes in vascular reactivity of the thoracic aorta and the coronary artery in the perfused heart of the d-SG-null mutant mouse model. Methods: Female knockout (KO) and wild-type (WT) mice (5 months old) with and without nitric oxid and prostanoids antagonist were used. Curves doses response to phenylephrine, angiotensin II and acetylcholine were constructed. Results: The results shows an increment in the contractile response to angiotensin II in the aorta and the isolated heart from the KO mice, and it seems due to a major participation of prostanoids. On the other hand the relaxant effect of acetylcholine is less in the KO than in the WT mice. Conclusion: Changes in vascular reactivity in KO mice seems due to the participation of prostanoids instead of nitric oxide.
Original languageAmerican English
Pages (from-to)322-330
Number of pages288
JournalPhysiology and Pharmacology (Iran)
StatePublished - 1 Dec 2017

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Sarcoglycans
Thoracic Aorta
Knockout Mice
Prostaglandins
Blood Vessels
Coronary Vessels
Angiotensin II
Acetylcholine
Phenylephrine
Genes
Smooth Muscle
Aorta
Myocardium
Nitric Oxide
Skeletal Muscle
Pharmacology
Mutation

Cite this

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title = "Changes in vascular reactivity of the coronary artery and thoracic aorta in the delta sarcoglycan null mutant mice",
abstract = "{\circledC} 2017, Iranian Society of Physiology and Pharmacology. All rights reserved. Introduction: Mutations in the delta sarcoglycan gene (d-SG) cause limb-girdle muscular dystrophy type 2F with structural and functional alterations in cardiac, smooth and skeletal muscle. The objective of the present study was to improve information about changes in vascular reactivity of the thoracic aorta and the coronary artery in the perfused heart of the d-SG-null mutant mouse model. Methods: Female knockout (KO) and wild-type (WT) mice (5 months old) with and without nitric oxid and prostanoids antagonist were used. Curves doses response to phenylephrine, angiotensin II and acetylcholine were constructed. Results: The results shows an increment in the contractile response to angiotensin II in the aorta and the isolated heart from the KO mice, and it seems due to a major participation of prostanoids. On the other hand the relaxant effect of acetylcholine is less in the KO than in the WT mice. Conclusion: Changes in vascular reactivity in KO mice seems due to the participation of prostanoids instead of nitric oxide.",
author = "Castillo-Hernandez, {Maria C.} and Gustavo Guevara-Balcazar and Alexandre Kormanovski and Gayosso, {Ivan Rubio} and Coral-Vazquez, {Ramon M.}",
year = "2017",
month = "12",
day = "1",
language = "American English",
pages = "322--330",
journal = "Physiology and Pharmacology (Iran)",
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TY - JOUR

T1 - Changes in vascular reactivity of the coronary artery and thoracic aorta in the delta sarcoglycan null mutant mice

AU - Castillo-Hernandez, Maria C.

AU - Guevara-Balcazar, Gustavo

AU - Kormanovski, Alexandre

AU - Gayosso, Ivan Rubio

AU - Coral-Vazquez, Ramon M.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - © 2017, Iranian Society of Physiology and Pharmacology. All rights reserved. Introduction: Mutations in the delta sarcoglycan gene (d-SG) cause limb-girdle muscular dystrophy type 2F with structural and functional alterations in cardiac, smooth and skeletal muscle. The objective of the present study was to improve information about changes in vascular reactivity of the thoracic aorta and the coronary artery in the perfused heart of the d-SG-null mutant mouse model. Methods: Female knockout (KO) and wild-type (WT) mice (5 months old) with and without nitric oxid and prostanoids antagonist were used. Curves doses response to phenylephrine, angiotensin II and acetylcholine were constructed. Results: The results shows an increment in the contractile response to angiotensin II in the aorta and the isolated heart from the KO mice, and it seems due to a major participation of prostanoids. On the other hand the relaxant effect of acetylcholine is less in the KO than in the WT mice. Conclusion: Changes in vascular reactivity in KO mice seems due to the participation of prostanoids instead of nitric oxide.

AB - © 2017, Iranian Society of Physiology and Pharmacology. All rights reserved. Introduction: Mutations in the delta sarcoglycan gene (d-SG) cause limb-girdle muscular dystrophy type 2F with structural and functional alterations in cardiac, smooth and skeletal muscle. The objective of the present study was to improve information about changes in vascular reactivity of the thoracic aorta and the coronary artery in the perfused heart of the d-SG-null mutant mouse model. Methods: Female knockout (KO) and wild-type (WT) mice (5 months old) with and without nitric oxid and prostanoids antagonist were used. Curves doses response to phenylephrine, angiotensin II and acetylcholine were constructed. Results: The results shows an increment in the contractile response to angiotensin II in the aorta and the isolated heart from the KO mice, and it seems due to a major participation of prostanoids. On the other hand the relaxant effect of acetylcholine is less in the KO than in the WT mice. Conclusion: Changes in vascular reactivity in KO mice seems due to the participation of prostanoids instead of nitric oxide.

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