Through this GABA dependent mechanism, with increased release of GABA within the NTS and, indirectly, reduced release from GABA by CVLM neurons, Ang II can interfere with short term blood pressure fluctuations, but could also lead to a baroreceptor resetting within the NTS resulting in an upregulation of the activity of the RVLM neurons and development of hypertension. The gene discussed is AGT; the disease is hypertensive disorder.