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Therapeutic Relevance Of AT2 Receptors In Cardiovascular Disease And Aging
Funder
National Health and Medical Research Council
Funding Amount
$519,279.00
Summary
Pharmacological modulation of the renin angiotensin system is a cornerstone of evidence-based cardiovascular therapeutics. However, their molecular mechanisms are not entirely clear and some therapeutic options have not been utilized to their full potential. The hormone angiotensin II causes both excitatory and inhibitory cardiovascular effects via distinct binding sites. Of particular importance to contemporary society is the shift in the demographic to a more aged population. In Australia in 2 ....Pharmacological modulation of the renin angiotensin system is a cornerstone of evidence-based cardiovascular therapeutics. However, their molecular mechanisms are not entirely clear and some therapeutic options have not been utilized to their full potential. The hormone angiotensin II causes both excitatory and inhibitory cardiovascular effects via distinct binding sites. Of particular importance to contemporary society is the shift in the demographic to a more aged population. In Australia in 2002, 13% of the population (~2.5 million) were aged 65 years or over, and it has been estimated that this number will increase to 18% (~4 million) by the year 2021. While lipid status and smoking are well known risk factors for cardiovascular disease, advanced age by far confers the greatest risk for cardiovascular disease. In this context, we have found a greater role of the inhibitory angiotensin II binding site in aging that may result from breakdown products of angiotensin II having their own unique effects. This project will determine the relative role of various angiotensin products, and novel compounds that may act similarly, to improve vascular tone and reverse cardiovascular disease in the elderly, hypertensive population.Read moreRead less
Anti-atherosclerotic Effects Of Angiotensin Fragments & Non-AT1 Receptors: Validation As Innovative Therapeutic Targets
Funder
National Health and Medical Research Council
Funding Amount
$512,065.00
Summary
In Australia the largest cause of death is coronary heart disease (CHD) leading to heart attacks or stroke and claiming a staggering 28,000 lives a year. Atherosclerosis is one of the leading causes of cardiovascular disease, with diseased vessels not able to fully dilate and the plaque that has built up inside these vessels impeding blood flow and possibly rupturing, resulting in heart attacks and stroke. One of the major players in the development and progression of atherosclerosis is the horm ....In Australia the largest cause of death is coronary heart disease (CHD) leading to heart attacks or stroke and claiming a staggering 28,000 lives a year. Atherosclerosis is one of the leading causes of cardiovascular disease, with diseased vessels not able to fully dilate and the plaque that has built up inside these vessels impeding blood flow and possibly rupturing, resulting in heart attacks and stroke. One of the major players in the development and progression of atherosclerosis is the hormone, angiotensin II. Angiotensin II has been found to trigger many factors that cause thickening of the vessel wall, inflammation and imbalances in vasodilator capacity (e.g. oxidative stress and endothelial dysfunction), all of which contribute to atherosclerosis. Clinical trials with drugs that inhibit the formation of angiotensin II (ACE inhibitors), or block the action of angiotensin II (angiotensin receptor antagonists), have demonstrated a significant decrease in mortality in patients with high risk for cardiovascular disease. However their mechanism(s) of action are not fully understood as the circulating levels of shorter fragments of angiotensin II (such as Ang IV and Ang (1-7)) are raised in the blood when these drugs are used and may contribute to the protective effects of these drugs. Importantly, we have found that both Ang IV and Ang (1-7) have protective effects in atherosclerotic blood vessels. Therefore, we hypothesise that fragments of angiotensin II (such as Ang IV and others) exert anti-atherogenic effects via distinct binding sites that oppose the effects caused by angiotensin II, and that these may be partly responsible for the cardio-protective effects of the ACE inhibitors and angiotensin receptor antagonists. Thus, information gained in our study will be useful in directing future prescription practices in clinical management of CHD and stroke, and for designing new therapeutic compounds for the management of atherosclerosis.Read moreRead less
Molecular Regulation Of The Type 1 Angiotensin Receptor
Funder
National Health and Medical Research Council
Funding Amount
$695,440.00
Summary
Angiotensin II is a hormone made in our bodies in response to a decrease in blood pressure (or salt in our bloodstream). It causes our blood vessels to constrict, makes us thirsty, and induces salt and fluid retention via an effect on the kidneys, thereby increasing blood pressure. In some cardiovascular diseases, the generation of angiotensin II or our sensitivity to this hormone is elevated. It is therefore crucial that we understand how angiotensin II works and how its actions in the body are ....Angiotensin II is a hormone made in our bodies in response to a decrease in blood pressure (or salt in our bloodstream). It causes our blood vessels to constrict, makes us thirsty, and induces salt and fluid retention via an effect on the kidneys, thereby increasing blood pressure. In some cardiovascular diseases, the generation of angiotensin II or our sensitivity to this hormone is elevated. It is therefore crucial that we understand how angiotensin II works and how its actions in the body are mediated. For angiotensin II to act it must first bind to a receptor. Receptors are proteins and behave like locks that are opened by the hormone keys. Thus, cellular receptors for angiotensin II are engaged and activated by increases in angiotensin II in our blood. These receptors then produce signals which initiate a response (e.g. constriction of a blood vessel). Subsequently, the receptors are switched-off to prevent over-stimulation. The experiments proposed in this application continue our investigations into how angiotensin II receptors are switched-on and -off. A major way for receptors to be turned on is for them to interact with other cellular proteins, although we know only some of these interactions for the angiotensin receptor. Receptors are turned off by being ear-marked by a modification known as phosphorylation; these modified receptors are then bound by proteins termed arrestins, which as indicated by their name, play a role in preventing further receptor signalling. These arrestins also help to remove activated receptors from the cell surface to the inside of the cell. This application proposes new technologies to investigate the spectrum of proteins recruited to the angiotensin receptor and the role of arrestins in switching receptors on and off. Results from these studies will further our understanding of angiotensin II receptors and their role in cardiovascular control.Read moreRead less
Helix VIII Of G Protein Coupled Receptors Is A Lipid-activated Signalling Sensor
Funder
National Health and Medical Research Council
Funding Amount
$389,250.00
Summary
G protein-coupled receptors (GPCRs) are the largest superfamily of membrane-embedded receptors and represent prime targets for drug development. The molecular basis for their activation and regulation is poorly understood, particularly the contribution of the membrane environment to receptor function. Using a range of molecular and biophysical approaches and the angiotensin receptor as a model GPCR, studies are proposed to understand the role of the cell membrane in GPCR activation. The results ....G protein-coupled receptors (GPCRs) are the largest superfamily of membrane-embedded receptors and represent prime targets for drug development. The molecular basis for their activation and regulation is poorly understood, particularly the contribution of the membrane environment to receptor function. Using a range of molecular and biophysical approaches and the angiotensin receptor as a model GPCR, studies are proposed to understand the role of the cell membrane in GPCR activation. The results will provide important new information on the molecular mechanism of GPCR regulation and exciting new approaches for drug design.Read moreRead less