Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol

Abstract While it is known that dilation of cerebral arterioles to NOS‐dependent agonists is impaired in rats exposed to prenatal alcohol, no studies have examined the influence of prenatal alcohol on constrictor response of cerebral arterioles. Our goal was to determine whether constrictor response...

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Autores principales: Partha S. Saha, Tiffany M. Knecht, Denise M. Arrick, Michael J. Watt, Jamie L. Scholl, William G. Mayhan
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Publicado: Wiley 2021
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spelling oai:doaj.org-article:21eb75ca20344f4cb5e75c9c51d88aed2021-11-15T09:54:40ZConstrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol2051-817X10.14814/phy2.15079https://doaj.org/article/21eb75ca20344f4cb5e75c9c51d88aed2021-11-01T00:00:00Zhttps://doi.org/10.14814/phy2.15079https://doaj.org/toc/2051-817XAbstract While it is known that dilation of cerebral arterioles to NOS‐dependent agonists is impaired in rats exposed to prenatal alcohol, no studies have examined the influence of prenatal alcohol on constrictor response of cerebral arterioles. Our goal was to determine whether constrictor responses of cerebral resistance arterioles are altered by prenatal exposure to alcohol and if any changes differed as a function of age or sex. We fed Sprague‐Dawley rat dams a liquid diet with or without alcohol (3% ethanol) for the duration of their pregnancy. We then examined reactivity of cerebral arterioles to thromboxane (U‐46619; 0.01 and 0.1 µM), arginine vasopressin (0.1 and 1 nM), and angiotensin II (1 and 10 µM) in four groups of offspring: control male and female, and prenatal alcohol male and female at two different ages (adolescent: 4–6 weeks old and adult: 14–16 weeks old). Constriction of cerebral arterioles to U‐46619 and AVP were similar in male and female rats regardless of exposure to prenatal alcohol and age. Similarly, adolescent male and female rats showed no difference to angiotensin II following prenatal exposure to alcohol. However, alcohol‐exposed females exhibited an unexpected dilation to the high concentration of angiotensin II in adulthood, which was absent in males. We suggest that the findings from these studies may have implications regarding the susceptibility of the brain to cerebral ischemic damage. We speculate that impaired vasodilation, coupled with preserved vasoconstriction, can lead to a scenario favoring a decrease in cerebral blood flow during times of increased metabolic demand.Partha S. SahaTiffany M. KnechtDenise M. ArrickMichael J. WattJamie L. SchollWilliam G. MayhanWileyarticlecerebral ischemiafetal alcohol syndromestrokevasoconstrictionPhysiologyQP1-981ENPhysiological Reports, Vol 9, Iss 21, Pp n/a-n/a (2021)
institution DOAJ
collection DOAJ
language EN
topic cerebral ischemia
fetal alcohol syndrome
stroke
vasoconstriction
Physiology
QP1-981
spellingShingle cerebral ischemia
fetal alcohol syndrome
stroke
vasoconstriction
Physiology
QP1-981
Partha S. Saha
Tiffany M. Knecht
Denise M. Arrick
Michael J. Watt
Jamie L. Scholl
William G. Mayhan
Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
description Abstract While it is known that dilation of cerebral arterioles to NOS‐dependent agonists is impaired in rats exposed to prenatal alcohol, no studies have examined the influence of prenatal alcohol on constrictor response of cerebral arterioles. Our goal was to determine whether constrictor responses of cerebral resistance arterioles are altered by prenatal exposure to alcohol and if any changes differed as a function of age or sex. We fed Sprague‐Dawley rat dams a liquid diet with or without alcohol (3% ethanol) for the duration of their pregnancy. We then examined reactivity of cerebral arterioles to thromboxane (U‐46619; 0.01 and 0.1 µM), arginine vasopressin (0.1 and 1 nM), and angiotensin II (1 and 10 µM) in four groups of offspring: control male and female, and prenatal alcohol male and female at two different ages (adolescent: 4–6 weeks old and adult: 14–16 weeks old). Constriction of cerebral arterioles to U‐46619 and AVP were similar in male and female rats regardless of exposure to prenatal alcohol and age. Similarly, adolescent male and female rats showed no difference to angiotensin II following prenatal exposure to alcohol. However, alcohol‐exposed females exhibited an unexpected dilation to the high concentration of angiotensin II in adulthood, which was absent in males. We suggest that the findings from these studies may have implications regarding the susceptibility of the brain to cerebral ischemic damage. We speculate that impaired vasodilation, coupled with preserved vasoconstriction, can lead to a scenario favoring a decrease in cerebral blood flow during times of increased metabolic demand.
format article
author Partha S. Saha
Tiffany M. Knecht
Denise M. Arrick
Michael J. Watt
Jamie L. Scholl
William G. Mayhan
author_facet Partha S. Saha
Tiffany M. Knecht
Denise M. Arrick
Michael J. Watt
Jamie L. Scholl
William G. Mayhan
author_sort Partha S. Saha
title Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
title_short Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
title_full Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
title_fullStr Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
title_full_unstemmed Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
title_sort constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol
publisher Wiley
publishDate 2021
url https://doaj.org/article/21eb75ca20344f4cb5e75c9c51d88aed
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