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Am J Physiol Heart Circ Physiol (October 21, 2004). doi:10.1152/ajpheart.00839.2004
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Submitted on August 18, 2004
Accepted on October 18, 2004

Angiogenic Protection from Focal Ischemia with Angiotensin II Type 1 Receptor Blockade in the Rat

Joan P. Forder1, Diane H. Munzenmaier1, and Andrew S. Greene2*

1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Biotechnology and Bioengineering Center, Medical College of Wisconsin, Milwaukee, WI, USA

* To whom correspondence should be addressed. E-mail: agreene{at}mcw.edu.

Angiogenesis within an ischemic region of the brain may increase tissue viability and act to limit the extent of an infarct. The angiotensin II pathway can both stimulate and inhibit angiogenesis depending on the tissue and activated receptors. Previous work has shown two week losartan administration (AT1 receptor blockade) initiates a significant cerebral angiogenic response. We hypothesized that administration of losartan in the drinking water of rats for two weeks prior to initiation of focal ischemia would decrease the extent of the resulting infarct. Adult male Sprague Dawley (SD) rats were given losartan (50mg/day) in their drinking water for two weeks prior to initiation of cerebral focal ischemia produced by cauterization of cortical surface vessels. Controls received normal drinking water. In control animals, three main vessels feeding the whisker barrel cortex (WBC) were cauterized resulting in cessation of blood flow. The same protocol was followed for losartan-treated animals but did not result in cessation of blood flow in WBC. Another group of losartan-treated animals received between 8-14 cauterizations of surface vessels feeding WBC and cessation of blood flow was verified. Rats were sacrificed 72h post-surgery. Morphological examination revealed angiogenesis, maintained vascular delivery, and significantly decreased infarct size in losartan-treated animals compared to control. These results demonstrate that pretreatment with losartan reduces infarct size following cerebral focal ischemia and supports the hypothesis that cerebral angiogenesis may be one of the mechanisms responsible.




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