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Am J Physiol Regul Integr Comp Physiol (January 18, 2007). doi:10.1152/ajpregu.00761.2005
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Submitted on October 27, 2005
Accepted on January 10, 2007

Comparative changes in the blood-brain barrier and cerebral infarction of SHR and WKY rats

Sharon Hom1, Melissa A Fleegal2, Richard D Egleton2, Christopher R Campos2, Brian T Hawkins2, and Thomas P. Davis1*

1 Pharmacology, University of Arizona, Tucson, Arizona, United States; Program in Physiological Sciences, University of Arizona, Tucson, Arizona, United States
2 Pharmacology, University of Arizona, Tucson, Arizona, United States

* To whom correspondence should be addressed. E-mail: davistp{at}u.arizona.edu.

Hypertension is involved in the exacerbation of stroke. It is unclear how blood-brain barrier (BBB) tight junction (TJ) and ion transporter proteins critical for maintaining brain homeostasis contribute to cerebral infarction during hypertension development. In the present study, we investigated cerebral infarct volume following permanent 4 hr middle cerebral artery occlusion (MCAO) and characterized the expression of BBB TJ and ion transporter proteins in brain microvessels of spontaneously hypertensive rats (SHR) compared to age-matched Wistar-Kyoto rats (WKY) at 5 (pre-hypertension), 10 (early stage hypertension) and 15 (later stage hypertension) weeks of age. Hypertensive SHR show increased infarct volume following MCAO as compared to WKY control. BBB TJ and ion transporter proteins, known to contribute to edema and fluid volume changes in the brain, show differential protein expression patterns during hypertension development. Western blot analysis of TJ protein zonula occludens-2 (ZO-2) showed decreased expression while ion transporter, Na+/H+ exchanger 1 (NHE-1), was markedly increased in hypertensive SHR. Expression of TJ proteins ZO-1, occludin, actin, claudin-5, and Na+/K+/2Cl- cotransporter (NKCC) remain unaffected in SHR compared to control. Selective inhibition of NHE-1 using dimethylamiloride (DMA) significantly attenuated ischemia-induced infarct volume in hypertensive SHR following MCAO, suggesting a novel role for NHE-1 in the brain in the regulation of ischemia-induced infarct volume in SHR.




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