Developmental programming of cardiorespiratory physiology
Developmental programming has the ability to change physiological function. We recently demonstrated changes in sympathetic nerve innervation and activity that would predispose in later life to hypertension. Developmental programming is also linked to a multitude of other cardiovascular pathologies such as obesity and diabetes. Combining animal models of developmental programming and lifecourse interventions allows us to investigate the mechanisms behind these pathologies.
Our research group has a wide range of experience ranging from carotid body function to sympathetic control of blood flow to help understand how developmental programming changes the phenotype of an animal and predisposes it to particular disease states.
In this study we will extend our work on the developmental programming induced by hypoxia in utero and will utilise a full range of experimental approaches from in vitro recording preparations to in vivo models with a limited potential of also investigating in human subjects. This studentship would suit high quality applicants who have an interest in integrative physiology and wish to develop their research skills in a stimulating environment. Applicants should hold or realistically expect to obtain at least an Upper Second Class Honours Degree in a subject linked to physiology.
How to apply
Informal enquiries should be directed to Dr Andrew Coney ([Email Address Removed])
To be considered for the studentship, please send the following documents to [Email Address Removed]:
• A detailed CV;
• Names and addresses of two referees;
• A covering letter highlighting your research experience/capabilities;
• Copies of your degree certificates with transcripts;
• Evidence of your proficiency in the English language, if applicable.
Thompson EL et al (2016). Adrenaline release evokes hyperpnoea and an increase in ventilatory CO2 sensitivity during hypoglycaemia: a role for the carotid body. J. Physiol. DOI: 10.1113/JP272191
Rook W et al (2014). Prenatal hypoxia leads to increased muscle sympathetic nerve activity, sympathetic hyperinnervation, blunting of neuropeptide Y signaling and hypertension in adult life. Hypertension 64:1321-1327. DOI: 10.1161/HYPERTENSIONAHA.114.04374
Marshall JM & Ray CJ (2012). Contribution of non-endothelium-dependent substances to exercise hyperaemia: are they O2 dependent? J. Physiol. 590:6307-6320. DOI: 10.1113/jphysiol.2012.240721