Laboratories

Baldi

The healthy heart can increase cardiac output 4 - 8-fold. This, combined with increased extraction of arterial oxygen by peripheral tissues, allows a 10 - 15-fold increase in oxygen consumption during peak exercise. Diabetes attenuates these cardiovascular responses and reduces aerobic capacity, an important prognostic indicator. We aim to determine why diabetes impairs the cardiovascular exercise response so that therapeutic interventions can be developed. Current projects are examining 1) the role of β-adrenergic dys-regulation in impaired cardiovascular responses, 2) the ability of glycaemic control and/or exercise training to improve these responses and 3) how changes in myocardial protein expression affect the performance of the diabetic heart. Animal studies are conducted with collaborators in the Department of Physiology and human studies involve collaborations with clinical staff in the Dunedin School of Medicine.

Chris Baldi

Chris Baldi

Dr Luke  Wilson

Luke Wilson

Genevieve Wilson

Genevieve Wilson

Erickson

Jeff Erickson

Jeff Erickson

Rachel Wallace

Rachel Wallace

Heather

Professor Alison Heather

Alison Heather

Jones

Calcium is the driving force behind every beat of the heart as every beat is the result of the careful movement, or cycling, of calcium in and out of each cell in the heart. Occasionally this carefully co-ordinated cycling of calcium goes wrong and this leads to lethal cardiac arrhythmias and cardiomyopathies. Our research is focused on better understanding the proteins responsible for the cycling of calcium in order to understand what goes wrong in cardiac disease. In particular we study the protein responsible for the release of calcium into each cell, the cardiac ryanodine receptor (RyR2). We are currently determining the changes to this protein in heart disease and are exploring how these changes result in altered calcium cycling and ultimately cardiac disease. This is achieved using a broad spectrum of assays from molecular biology and single channel recordings, through to isolated cardiac myocytes (from animals and patients) and ultimately whole animal models.

Dr Peter Jones

Peter Jones

Gillian Hughes

Gillian Hughes

Janet McLay

Janet McLay

Helen Waddell

Helen Waddell

Joe Zhang

Joe Zhang

Katare

Dr Rajesh Katare

Rajesh Katare

Midori Edamatsu

Midori Edamatsu

Ingrid Fomison-Nurse

Ingrid Fomison-Nurse

Andrew Moore

Andrew Moore

Pujika Munasinghe

Pujika Munasinghe

Thrishila Parshu Ram

Thrishila Parshu Ram

Shruti Rawal

Shruti Rawal

Amol Shindikar

Amol Shindikar

Lamberts

Sympathetic activation is the basis for the stress-induced fight-or-flight response. Normal physiological effects of sympathetic activation on the heart are a stronger contraction and a faster heart rate. The sympathetic input to the heart, via cardiac sympathetic nerve activity (synaptic release of noradrenaline) and via circulating adrenaline act on different adrenoceptor subtypes on the heart determining it responsiveness. During long-term metabolic stress, like in obesity and diabetes, the sympathetic activation mechanism is changed, however it is unknown exactly how. One of the consequences could be that obese and diabetic patients are less capable of coping with the short-term perioperative stress during surgery, which would explain their increased risk of cardiovascular complications and their worst outcome after surgery. Therefore, I aim to determine the regulation of cardiac function by catecholamines under stressful conditions, such as obesity, diabetes and perioperative stress. By generating basic biomedical data at molecular, cellular, and whole-animal in vivo level, and combining this with human cardiac tissue studies to translate it to the clinical setting, I aim to unveil the responsible unidentified signalling mechanisms.

Dr Regis Lamberts

Regis Lamberts

Carol Bussey

Carol Bussey

Rosalind Cook

Rosalind Cook

Lorna Daniels

Lorna Daniels

Gillian Hughes

Gillian Hughes

Schwenke

The functional capacity of the heart relies heavily on input from the autonomic nervous system to cope with the large and dynamic changes in cardiac output. In particular, sympathetic nerve activity provides the robust increase in cardiac performance in preparation for the 'fight-or-flight' response. Following an acute myocardial infarction, however, increases in sympathetic activity become counterintuitive dangerous for the heart, as it provides an extrinsic trigger for potentially-fatal arrhythmias. Yet surprisingly the pathomechanisms that underpin this dangerous increase in sympathetic activity remains to be fully elucidated. My research aims to identify central and peripheral pathways that contribute to the increase in sympathetic activity following acute myocardial infarction and, moreover, assess potential therapeutic strategies for ameliorating sympathetic excitation; in particular, the therapeutic potential of ghrelin.

Dr Daryl Schwenke

Daryl Schwenke

Natalie Joe

Natalie Joe

Chris Baldi

Chris Baldi

My general area of research is to examine the causes and prevention of cardiovascular dysfunction in patients with diabetes (type 1 and 2). Interests include: Exercise intolerance in diabetes; Myocardial and pulmonary dysfunction in diabetes; Paediatric diabetes research.

Email: chris.baldi@otago.ac.nz

Dr Luke Wilson

Luke Wilson

Teaching Fellow

Phone: +64 3 4795602

Email: luke.wilson@otago.ac.nz

Genevieve Wilson

Genevieve Wilson

BSc Honours Student

Email: wilge046@student.otago.ac.nz

Jeff Erickson

Jeff Erickson

Lecturer

My research focuses on investigating the molecular mechanisms that underlie structural heart disease and heart failure, particularly in the context of aging and diabetes.

Phone: +64 3 4703414

Email: jeff.erickson@otago.ac.nz

Rachel Wallace

Rachel Wallace

Assistant Research Fellow

Email: rachel.wallace.otago.ac.nz

Professor Alison Heather

Alison Heather

Professor

Phone: 479 7399

Email: alison.heather@otago.ac.nz

Dr Peter Jones

Peter Jones

Senior Lecturer

My principal research interest is in how calcium cycling is controlled in cardiac myocytes. In particular my focus is on the mechanisms by which calcium release from intra-cellular stores (sarcoplasmic reticulum, SR) is controlled by the cardiac ryanodine receptor (RyR2). The aim of my research is to characterise how the activity of RyR2 is altered both physiologically and in disease. This is achieved using a broad spectrum of assays from molecular biology and single channel recordings, through to isolated cardiac myocytes and ultimately whole animal models.

Phone: +64 3 4703548

Email: pete.jones@otago.ac.nz

Gillian Hughes

Gillian Hughes

Assistant Research Fellow

Phone: +64 3 4703417

Email: gill.hughes@otago.ac.nz

Janet McLay

Janet McLay

Research Technician

Phone: +64 3 4794211

Email: janet.mclay@otago.ac.nz

Helen Waddell

Helen Waddell

Research Assistant

The effect of oxidation on cardiac ryanodine receptor function

Phone: +64 3 4794211

Email: wadhe186@student.otago.ac.nz

Joe Zhang

Joe Zhang

PhD Student

Regulation of the cardiac ryanodine receptor.

Phone: +64 3 4794211

Email: zhazh623@student.otago.ac.nz

Dr Rajesh Katare

Rajesh Katare

Senior Lecturer

Phone: +64 3 4797292

Email: rajesh.katare@otago.ac.nz

Midori Edamatsu

Midori Edamatsu

Visiting Student

Phone: +64 3 4703417

Ingrid Fomison-Nurse

Ingrid Fomison-Nurse

Assistant Research Fellow

Phone: +64 3 4797512

Email: ingrid.fomison-nurse@otago.ac.nz

Andrew Moore

Andrew Moore

PGDipSci student

Why do females have higher risk of diabetic heart disease?

Phone: +64 3 4797512

Email: mooan627@student.otago.ac.nz

Pujika Munasinghe

Pujika Munasinghe

Visiting Student

Phone: +64 3 4797512

Thrishila Parshu Ram

Thrishila Parshu Ram

BSc Honours Student

Pathophysiology of microRNAs in diabetic hearts

Phone: +64 3 4797512

Email: parth848@student.otago.ac.nz

Shruti Rawal

Shruti Rawal

PhD Student

Pathological role of microRNAs in the development of diabetic heart disease

Phone: +64 3 4797512

Email: shr25175@student.otago.ac.nz

Amol Shindikar

Amol Shindikar

Assistant Research Fellow

Phone: +64 3 4797512

Email: amol.shindikar@otago.ac.nz

Dr Regis Lamberts

Regis Lamberts

Senior Lecturer

Phone: +64 3 4703547

Email: regis.lamberts@otago.ac.nz

Carol Bussey

Carol Bussey

Assistant Research Fellow

Phone: +64 3 4796371

Email: carol.bussey@otago.ac.nz

Rosalind Cook

Rosalind Cook

PhD Student

Adrenergic modulation of the diabetic heart

Phone: +64 3 4703417

Email: cooro724@student.otago.ac.nz

Lorna Daniels

Lorna Daniels

PhD Student

Email: danlo676@student.otago.ac.nz

Gillian Hughes

Gillian Hughes

Assistant Research Fellow

Phone: +64 3 4703417

Email: gill.hughes@otago.ac.nz

Dr Daryl Schwenke

Daryl Schwenke

Senior Lecturer

The functional capacity of the heart relies heavily on input from the autonomic nervous system to cope with the large and dynamic changes in cardiac output. In particular, sympathetic nerve activity provides the robust increase in cardiac performance in preparation for the 'fight-or-flight' response. Following an acute myocardial infarction, however, increases in sympathetic activity become counterintuitive dangerous for the heart, as it provides an extrinsic trigger for potentially-fatal arrhythmias. Yet surprisingly the pathomechanisms that underpin this dangerous increase in sympathetic activity remains to be fully elucidated. My research aims to identify central and peripheral pathways that contribute to the increase in sympathetic activity following acute myocardial infarction and, moreover, assess potential therapeutic strategies for ameliorating sympathetic excitation; in particular, the therapeutic potential of ghrelin.

Phone: +64 3 4797330

Email: daryl.schwenke@otago.ac.nz

Natalie Joe

Natalie Joe

Assistant Research Fellow

Phone: +64 3 4796371

Email: natalie.joe@otago.ac.nz

HeartOtago operates with funding from the following organisations:
University of Otago Research GrantOtago Medical Research FoundationMarsden FundLottery Health ResearchHeart FoundationHealthcare Otago Trust