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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2021
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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) |
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cerebral ischemia fetal alcohol syndrome stroke vasoconstriction Physiology QP1-981 |
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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 |
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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 |
work_keys_str_mv |
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