Expression of AT1, AT2 receptors and a non-AT1, non-AT2 angiotensin II binding site in rat brain after endothelin-1 induced ischemic stroke

Expression of AT1, AT2 receptors and a non-AT1, non-AT2 angiotensin II binding site in rat brain after endothelin-1 induced ischemic stroke

New findings suggest that the activation AT1 receptor decreases cerebral perfusion after an ischemic stroke in the brain while the activation of AT2 receptor opposes those actions providing neuroprotective effects. Recent discoveries reveal the existence of a novel non-AT1, non-AT2 binding site for angiotensin II (Ang II) in the brain which may indicate additional effects of the brain angiotensin system after ischemic damage. To assess this, 5 rats were microinjected with 3 μl of 80 μM endothelin-1 (ET-1) to stimulate middle cerebral artery occlusion in the right hemisphere of the forebrain. 24 hours later, the rats were sacrificed and the brains were removed and frozen. The brains were analyzed by observing the binding of 125I-Sar1 Ile8 Ang II to the tissue by receptor autoradiography. Using quantitative densitometric analysis of the 125I-Sar1 Ile8 Ang II binding (MCID) to the forebrain caudal to the ischemic region of the brain, no differences in AT1, AT2 or non-AT1, non-AT2 binding was observed between the hemispheres in either the density of the receptor binding or the area encompassed by each hemisphere. The results suggest that the ischemia does not alter the expression of angiotensin binding proteins in the region posterior to the stroke zone at 24 hours post-ischemia.