<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(6)</volume><submitter>Dinh QN</submitter><pubmed_abstract>Aging is commonly associated with chronic low-grade inflammation and hypertension but it is unknown whether a cause-effect relationship exists between them. We compared the sensitivity of young adult (8-12 w) and aged (23-31 mo) male C57Bl6J mice to develop hypertension in response to a slow-pressor dose of angiotensin II (Ang II; 0.28 mg/kg/d; 28 d). In young mice, the pressor response to Ang II was gradual and increased to 142±8 mmHg over 28 d. However, in aged mice, Ang II promptly increased SBP and reached 155±12 mmHg by 28 d. Aging increased renal but not brain expression of Ang II receptors (&lt;i>At1ar&lt;/i> and &lt;i>At2r&lt;/i>) and elevated AT1R:AT2R expression ratio in mesenteric artery. Maximal contractile responses of mesenteric arteries to Ang II were enhanced in aged mice and were not </pubmed_abstract><journal>Aging</journal><pagination>1595-1606</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5509458</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Pressor response to angiotensin II is enhanced in aged mice and associated with inflammation, vasoconstriction and oxidative stress.</pubmed_title><pmcid>PMC5509458</pmcid><pubmed_authors>Chrissobolis S</pubmed_authors><pubmed_authors>Kemp-Harper BK</pubmed_authors><pubmed_authors>Vinh A</pubmed_authors><pubmed_authors>Diep H</pubmed_authors><pubmed_authors>Robertson AAB</pubmed_authors><pubmed_authors>Mansell A</pubmed_authors><pubmed_authors>Drummond GR</pubmed_authors><pubmed_authors>De Silva TM</pubmed_authors><pubmed_authors>Cooper MA</pubmed_authors><pubmed_authors>Dinh QN</pubmed_authors><pubmed_authors>Sobey CG</pubmed_authors><pubmed_authors>Kim HA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pressor response to angiotensin II is enhanced in aged mice and associated with inflammation, vasoconstriction and oxidative stress.</name><description>Aging is commonly associated with chronic low-grade inflammation and hypertension but it is unknown whether a cause-effect relationship exists between them. We compared the sensitivity of young adult (8-12 w) and aged (23-31 mo) male C57Bl6J mice to develop hypertension in response to a slow-pressor dose of angiotensin II (Ang II; 0.28 mg/kg/d; 28 d). In young mice, the pressor response to Ang II was gradual and increased to 142±8 mmHg over 28 d. However, in aged mice, Ang II promptly increased SBP and reached 155±12 mmHg by 28 d. Aging increased renal but not brain expression of Ang II receptors (&lt;i>At1ar&lt;/i> and &lt;i>At2r&lt;/i>) and elevated AT1R:AT2R expression ratio in mesenteric artery. Maximal contractile responses of mesenteric arteries to Ang II were enhanced in aged mice and were not </description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jun</publication><modification>2025-04-18T20:42:23.952Z</modification><creation>2019-03-27T02:50:22Z</creation></dates><accession>S-EPMC5509458</accession><cross_references><pubmed>28659507</pubmed><doi>10.18632/aging.101255</doi></cross_references></HashMap>