Principal investigators
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.
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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.
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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.
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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.
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