Effect of AT 1 receptor blockade on intermittent hypoxia-induced endothelial dysfunction

Noah J. Marcus, Nathan R. Philippi, Cynthia E. Bird, Yulong Li, Harold D Schultz, Barbara J. Morgan

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

Chronic intermittent hypoxia (CIH) raises arterial pressure, impairs vasodilator responsiveness, and increases circulating angiotensin II (Ang II); however, the role of Ang II in CIH-induced vascular dysfunction is unknown. Rats were exposed to CIH or room air (NORM), and a subset of these animals was treated with losartan (Los) during the exposure period. After 28 days, vasodilatory responses to acetylcholine or nitroprusside were measured in isolated gracilis arteries. Superoxide levels and Ang II receptor protein expression were measured in saphenous arteries. After 28 days, arterial pressure was increased and acetylcholine-induced vasodilation was blunted in CIH vs. NORM, and this was prevented by Los. Responses to nitroprusside and superoxide levels did not differ between CIH and NORM. Expression of AT 2R was decreased and the AT 1R:AT 2R ratio was increased in CIH vs. NORM, but this was unaffected by Los. These results indicate that the blood pressure elevation and endothelial dysfunction associated with CIH is dependent, at least in part, on RAS signaling.

Original languageEnglish (US)
Pages (from-to)67-74
Number of pages8
JournalRespiratory Physiology and Neurobiology
Volume183
Issue number2
DOIs
StatePublished - Aug 15 2012

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Keywords

  • Angiotensin II
  • Endothelial function
  • Intermittent hypoxia

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pulmonary and Respiratory Medicine

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