School of Medical Sciences

Circulatory Control Laboratory

Principal investigators

Lab group visiting the construction site
Lab group visiting the construction site of our new lab (Feb 2011)

Research interests

The focus of Circulatory Control Laboratory is the control of blood pressure with particular regard to the mechanisms responsible for the development of hypertension and other cardiovascular diseases. The main approach of the laboratory is an integrated approach of monitoring of a number of cardiovascular variables such as blood pressure, sympathetic nerve activity, heart rate and blood flow for an extended period of time. Interests include the role of the sympathetic nervous system in the genesis of hypertension and the development of heart failure following myocardial Infarction. The laboratory currently receives funding from the Auckland Medical Research Foundation and the Health Research Council. This funding supports two postdoctoral research fellows, one PhD student, one Masters student and two Honours students. The laboratory has active collaborations with research groups in Ireland, Australia and the United States, as well as having a close liaison with the Bioengineering Institute and "Telemetry Research Ltd" a company that has evolved as a result of our own research needs and now sells telemetry based physiological monitoring equipment throughout the world.

Current projects

Cardiovascular diseases are the leading cause of death in the developed world and increased sympathetic nerve activity generated by the brain occurs in almost all of these diseases.


SNA and hypertension

Increases in sympathetic nerve activity may be important in the development of hypertension, but little is known about how or why this translates to increased blood pressure. One possibility is that long-term increases in nerve activity alter the kidneys ability to excrete salt and regulate body-fluid. Using unique wireless monitoring equipment we have developed, we directly record sympathetic activity to the kidney during the development of hypertension. In particular we explore the interaction between dietary salt, hormones, nerve activity and blood pressure. The ultimate goal of this project is to gain an entirely new perspective for understanding the pathogenesis of hypertension in order to better target treatment interventions in humans to match the physiological changes occurring during the progression of the disease.


Heart failure following myocardial infarction

Myocardial infarction (MI) is a leading cause of death and disability in New Zealand. To date, the majority of drugs for both prevention of recurrent events and ameliorating adverse cardiac remodelling post-MI appear to operate by reducing neurohumoral activation. Elevation of renal SNA is thought to play a critical role in the volume retention seen in heart failure, which in turn increases the workload on the already compromised heart. Overall it is clear that activation of the renal nerves may be a key factor in pathology development after MI, yet we know very little about the reasons renal SNA becomes elevated after MI and its progression to heart failure. Several of our current projects examine the fundamental mechanisms leading to sympathetic activation and its control post-MI both in the short and long  term.


The effects of necrotic trophoblasts on maternal blood pressure control

Preeclampsia is a disorder specific to pregnancy resulting from maladaptation of the maternal control of blood pressure which leads to a range of symptoms including gestational hypertension which is characteristic of the disorder. The predominant theory of the cause of preeclamsia is that endothelial dysfunction precedes the onset of maternal hypertension and it is known that endothelial dysfunction is induced by a placental factor that is yet to be characterised. One of the placental factors proposed to cause preeclampsia are syncytial knots. Syncytial knots are of multi-nucleated fragments of the syncytiotrophoblast, the placental cell layer that forms the surface of the placenta and is bathed in maternal blood. Larry Chamley’s research group (Dept of Obstetrics and Gynaecology) have shown that endothelial cells can phagocytose dead syncytial knots. His research group have also shown that the phagocytosis of necrotic trophoblasts induces activation of the endothelial cells, which is also seen in endothelial dysfunction that precedes preeclampsia. Phagocytosis of apoptotic trophoblasts does not appear to have the same effects. In collaboration with Larry Chamley, this research project is based on the theory that phagocytosis of necrotic syncytial knots leads to an increase in blood pressure leading to preeclampsia and aims to test out specifically whether necrotic trophoblasts increase blood pressure.













Renal oxygen recording to investigate the progression of chronic kidney disease

Chronic kidney disease (CKD) is a global public health problem. It has been postulated that progression of CKD is partly due to disturbed kidney oxygenation, i.e. renal hypoxia. Yet we know little about the causes of renal hypoxia or how to treat it. The critical barrier to investigate this is the lack of methods to chronically measure kidney tissue oxygen. To force a breakthrough in linking hypoxia to impaired renal health, this project will realize a telemetry-based solution for chronic measurement of oxygen in the kidney. We hypothesize that a family of new telemetry-based electrochemical sensors will facilitate continuous recording of oxygen within kidney tissue over extended periods of time. This project will generate unique technology, knowledge and expertise to improve testing, validating and understanding of disturbed kidney oxygenation in chronic kidney disease.