They proposed that increased AT1 receptor binding in the RVLM might contribute to the hypertension of SHR, whereas reduced radioligand binding to the novel, non-AT1, non-AT2, angiotensin binding site in the RVLM of SHR might indicate a role for this binding site to reduce blood pressure via its interactions with Ang II and III. This evidence concerns the gene AGT and hypertensive disorder.