Central Cardiovascular Regulation Group
Key Findings |
Techniques |
Publications & Funding |
Prospective Students |
Lab Members
Andrew Allen- Senior Lecturer
Annabel Simms- Postdoctoral Fellow
Jaspreet Bassi- Research Assistant
Daian Chen- Ph.D. student (2007 -)
Nilanka Hettigoda- Ph.D. student (2008 -)
Erin O’Callaghan- Ph.D. student (2007-)
Charles Sevigny- Ph.D. student (2005- )
Research Interests
The group has an overarching interest in how the central nervous system modulates cardiovascular function via the autonomic nervous system. This encompasses an interest in neuroscience, particularly how neural groups interact in vivo to generate specific motor patterns (in this case sympathetic activity to vascular smooth muscle), as well as the cardiovascular system. The following sections describe a few of our main areas of current interest.
Current Interests
Understanding the brain renin-angiotensin system.
Whilst its existence was suggested over 30 years ago, the brain renin-angiotensin system remains incompletely understood. Is angiotensin generated within the brain? If so how does this happen when the constituents are present in different cell types (angiotensinogen in astrocytes; renin in very low concentration in some neurons)? Is angiotensin released from presynaptic terminals in response to depolarization- i.e. is it a neurotransmitter? These fundamental questions remain unanswered despite the fact that angiotensin is known to exert powerful actions in the brain on fluid and electrolyte homeostasis, autonomic activity and neuroendocrine function.
Which neural pathways are involved in cardiovascular diseases?
Neural regulation of sympathetic and parasympathetic activity is clearly altered in cardiovascular diseases such as hypertension and heart failure. In fact, alteration of this nervous activity is proposed to cause these diseases in some cases. Yet, the neural circuits that regulate sympathetic and parasympathetic activity are understood at only a superficial level- and then incompletely. We are attempting to understand more about this circuitry in order to test fundamental questions such as:
“Can a centrally-generated increase in sympathetic activity lead to sustained hypertension?”
“Can we modify the progression of cardiovascular diseases by altering neural function?”
To answer these questions we are performing:
- viral transduction studies to alter gene expression in specific groups of neurons.
- specific drug administration to alter activity of certain neuron groups.
How do neurons interact?
With an estimated 1 billion neurons in the brain and each neuron potentially receiving information from hundreds of other neurons the potential interactions are mind-boggling. Reduced preparations are commonly used to try and bring the scale of these interactions to understandable proportions. We are trying to understand the mechanisms by which one of the simpler mammalian neural circuits works to generate activity. This is the circuitry responsible for the generation of sympathetic activity to blood vessels. We now know the constituent members of the circuit and their function on a broad level. This then brings us to an exciting point where we can look at:
- how individual neurons generate tonic activity
- how local synaptic interactions modify function