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Angiotensin receptor gene expression in candesartan mediated neuroprotection

Qing Lu1, Yi-Zhun Zhu, Peter T-H Wong

  • 1Department of Pharmacology, Faculty of Medicine, National University of Singapore, 18 Medical Drive, Singapore 117597.

Neuroreport
|December 1, 2004
PubMed

Insights

Candesartan cilexetil (TCV-116) treatment lowered blood pressure and reduced stroke-related brain damage in rats. This suggests potential neuroprotective benefits mediated by AT1 receptor antagonism and AT2 receptor up-regulation.

Area of Science:

  • Cardiovascular Pharmacology
  • Neuroscience
  • Ischemic Stroke Research

Background:

  • The renin-angiotensin system plays a role in cardiovascular regulation and cerebrovascular function.
  • Angiotensin II exerts effects through AT1 and AT2 receptors, influencing blood pressure and potentially neuroprotection.
  • Candesartan cilexetil is an angiotensin AT1 receptor antagonist with known antihypertensive effects.

Purpose of the Study:

  • To investigate the effects of candesartan cilexetil (TCV-116) on blood pressure, AT2 receptor expression, and neuroprotection in a rat model of ischemic stroke.
  • To explore the potential mechanisms underlying the neuroprotective effects of TCV-116.

Main Methods:

  • Male Wistar rats were administered candesartan cilexetil (1 mg/kg/day) for 4 weeks.
  • Systolic blood pressure was monitored throughout the treatment period.
  • Gene expression of AT1 and AT2 receptors was analyzed.
  • Middle cerebral artery occlusion was induced to model ischemic stroke.
  • Infarct volume and neurological scores were assessed in treated and control rats.

Main Results:

  • TCV-116 significantly reduced systolic blood pressure by 14% within 1 week, with sustained effect.
  • A significant up-regulation of AT2 receptor gene expression (3.4-fold at 1 week, 5.0-fold at 4 weeks) was observed, while AT1 receptor expression remained unchanged.
  • TCV-116 treatment resulted in approximately 30% reduction in infarct volume compared to controls.
  • Treated rats showed improved neurological scores post-stroke.

Conclusions:

  • Candesartan cilexetil demonstrates significant antihypertensive effects and neuroprotective properties in a rat model of ischemic stroke.
  • The observed neuroprotection is potentially mediated by AT1 receptor antagonism coupled with the up-regulation of AT2 receptors.
  • These findings suggest a therapeutic role for candesartan cilexetil in managing ischemic stroke, possibly through modulation of the renin-angiotensin system.

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