Ventrolateral medulla in spontaneously hypertensive rats and the role of angiotensin 2

In this week’s blog, I reviewed a paper that studied the role of Angiotensin II in the ventrolateral medulla (VLM) in spontaneously hypertensive rats (SHR) and its contributions to cardiovascular regulation. Initially, Muratani et al, examined the VLM by microinjection of Angiotensin II antagonist into the rostral or ventral portion of the VLM. The antagonist caused a depressive effects and bradycardia in the RVLM, conversely, causing stimulating effects and tachycardia in the CVLM. Ultimately, blood pressure increased in SHR compared to the control group of normotensive rats. A group of 32 male rats between 14-16 week old were used in this study. Animals were anesthetized using urethan before injection. The results of this experiment indicated microinjections of Angiotensin II antagonist into the CVLM increased blood pressure and heart rate in SHR compared to normotensive rats. On the contrary, Angiontensin II antagonist injection into the RVLM produced a depressive response ultimately decreasing mean arterial pressure and heart rate. Therefore, angiontensin II receptor blockage in the VLM imply that angiotensin II has a tonic effect on the neural activity of the RVLM and CVLM of SHR. Furthermore, the results of this study show that brain Angiotensin II contribute to the continual regulation neural activity of the VLM and its regulation of the blood pressure.

This was an older paper that I read on angiotensin II and though it doesn’t directly relate to what I am currently working on, it did focus on the VLM and how different aspects can effect its regulation of blood pressure. Furthermore, since CV is the leading cause of death, it shows that continual research still must be conducted on this brain region to figure alternative ways to regulate on blood pressure and ultimately reduce the amount of deaths from CV.

Dean