Amygdala centralis cardiovascular response to angiotensin I microinjection in Goldblatt hypertensive rats



Previous studies have shown that induction of 2kidney -1clip Goldblatt hypertension (2K-1C) induction in rats eliminates hypertensive response after inactivating of the central nucleus of the amygdale (ACe). The present study investigated the possibility of alteration in local renin angiotensin system (RAS) activity in ACe after hypertension induction. Clamps were placed on the left renal arteries of a group of Wistar rats to induce 2K-1C Goldblatt hypertension. A similar surgery without clipping was done in sham group. Rats were studied six weeks after surgery. The mean arterial blood pressure (MAP) and heart rate (HR) were measured directly with indwelling arterial cannulas under urethane anesthesia. Rats received bilateral cannulation of the ACe for angiotensin I (AngI) microinjection. Before and 5,10,20,40 and 60 minutes after bilateral microinjection of Ang I (1 µL, 100 µM) into ACe, MAP and HR measured and compared between groups. In normotensive rats, significant changes in MAP or HR were not seen. Meanwhile, in hypertensive rats MAP significantly increased 5, 10, and 20 minutes after (p<0.05, p<0.05, p<0.01) though HR remained unaltered. MAP alteration range by microinjection in hypertensive rats has significantly been different in comparison with normotensive ones at mentioned times (p<0.05, p<0.01, p<0.05). This data shows that inhibitory effect of Ang I on ACe has increased after hypertension induction. This process may contribute in hypertension development. Increased Angiotensin II (Ang II) receptors or accelerated converting process of AngI to AngII may altere Ang I microinjection in ACe outcome.