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Cardiovascular Pharmacology Laboratory

Group Head

Dr Robert Widdop

BSc(Hons) PhD

Tel: +61 3 9905 4858 / 9905 2042
Fax: +61 3 9905 5851

Specific Interests

Haemodynamic actions of vasoactive peptides, particularly the renin-angiotensin system
Hypertension, heart failure & atherosclerosis
Acute & chronic cardiovascular effects of peptides & nonpeptide antagonists
Central and peripheral control of blood pressure
Cardiac & vascular remodelling during cardiovascular disease and its regression by drug treatment

Current projects

Our main area of interest is in the pharmacology of vasoactive peptides and, in particular, how their modulation (stimulation/inhibition) relate to the control of blood pressure and the pathophysiology of hypertension, congestive heart failure and atherosclerosis.

Our current projects involve the role of a number of angiotensin peptides, and of other peptides such as endothelin, in cardiovascular regulation. These peptides, together with selective nonpeptide antagonists and inhibitors are used in several animal models of hypertension (of both genetic and renal origin); an acute myocardial infarction model of heart failure, as well as in models of atherosclerosis and restenosis. Techniques used include regional haemodynamic (pulsed Doppler flow) measurements, blood pressure radiotelemetry for chronic studies, vasoactive and baroreflex testing. Ex vivo cardiac and vascular remodelling parameters (e.g. hypertrophy & fibrosis), as well as immunohistochemical localisation of a number of inflammatory mediators and receptor targets are also examined in the cardiovascular system following chronic manipulation of various peptidergic systems. In vitro reactivity of blood vessels from chronically treated animals is also examined.

Collaborative projects are also in progress with other members of Department and externally
(see below)

Members of Laboratory

Dr Tracey Gaspari, PhD (Research Officer, NHMRC)
Ms Iresha Welungoda, BSc (Hons) (Research Assistant, NHMRC)
Ms Ruth Hannan (PhD student)
Ms Emma Jones (PhD student, National Heart Foundation)
Mr Stuart McDougall (PhD student)
Ms Pia Walters (PhD student)
Ms Lisa Duke (PhD student)
Mr Antony Vinh (PhD student)

Current Collaborators

Dr Joanne Favaloro, PhD (Peter Doherty Fellow, NHMRC), Dept. Pharmacology, Monash Univ.
Role of reactive nitrogen species in vascular tone

Dr Jane Black, Dept. Anatomy & Cell Biology, Monash Univ.
Cardiac remodelling following inhibition of renin-angiotensin system

Dr Roger Evans, Dept. Physiology, Monash Univ.
Effects of angiotensin peptides on regional kidney blood flow

Dr Andrew Lawrence, Howard Florey Institute
Stress: cardiovascular function and central neurochemical modulation

Dr Anthony Zulli & A/Prof David Hare, Dept. Cardiology, Austin Hosptital, Univ. of Melbourne
Localisation of angiotensin receptor subtypes in human vasculature

Dr Anthony Dear, Box Hill Hospital, Monash University
A study of abdominal aortic aneurysms

Dr Daniel Henrion, INSERM, Paris VII University, Paris, France.
Functional role of angiotensin AT2 receptor in isolated vasculature

Recent selected publications

  • Zwart, A., Davis, E.A. and Widdop, R.E. (1998). Modulation of AT1 receptor-mediated contraction of rat uterine artery by AT2 receptors. Brit. J. Pharmacol., 125, 1429-1436.
  • Sampey, D.B., Burrell, L.M. and Widdop, R.E. (1999). Vasopressin V2 receptor enhances gain of baroreflex in conscious spontaneosly hypertensive rats. Am J. Physiol., 276, R872-R879.
  • Bunting, M.W. and Widdop, R.E. (1999). Differential haemodynamic effects of endothelin antagonist, SB 209670, in conscious hypertensive and normotensive rats. Eur. J. Pharmacol., 381, 13-21.
  • Widdop, RE, Sampey, DB and Jarrott, B (1999). Cardiovascular effects of angiotensin-(1-7) in conscious spontaneously hypertensive rats. Hypertension, 34 [part 2], 964-968.
  • Barber, M.N., Sampey, D.B. and Widdop, R.E. (1999). AT2 receptor stimulation enhances antihypertensive effect of AT1 receptor antagonist in hypertensive rats. Hypertension, 34, 1112-1116.
  • McDougall, S.J., Paull, J.R.A., Widdop, R.E. and Lawrence, A.J. (2000). Restraint stress: differential cardiovascular responses in WKY and SHR. Hypertension, 35, 126-129.
  • Paull, J.R.A., Li, X.C., Sampey, D.B. and Widdop, R.E. (2001). Pharmacodynamic contribution to the vasodilator effect of chronic AT1 receptor blockade in SHR. Hypertension, 37, 91-98.
  • Paull, J.R.A. and Widdop, R.E. (2001). Persistent cardiovascular effects of chronic renin-angiotensin system inhibition following withdrawal in adult SHR. J. Hypertension, 19, 1393-1402.
  • Widdop, RE, Matrougui, K, Levy, BI and Henrion, D. (2002). AT2 receptor-mediated relaxation is preserved after long-term AT1 receptor blockade. Hypertension, 40, 516-520.
  • Roulston CL, Lawrence AJ, Jarrott B & Widdop RE (2003). Localization of AT2 receptors in the nucleus of the solitary tract of spontaneously hypertensive and Wistar Kyoto rats using [125I] CGP42112: upregulation of a non-angiotensin II binding site following unilateral nodose ganglionectomy. Brain Research, 968, 139-155.
  • Duke, LM, Paull, JRA and Widdop, R.E. (2003). Cardiovascular status following combined angiotensin converting enzyme and AT1 receptor inhibition in conscious spontaneously hypertensive rats. Clin. Exp. Pharmacol. Physiol., 30, 317-323.
  • Duke LM, Eppel GA, Widdop RE & Evans RG (2003). Disparate roles of AT2 receptors in the renal cortical and medullary circulations of anaesthetized rabbits. Hypertension, 42, 200-205.
  • Zulli A, Widdop RE, Hare DL, Buxton BF & Black MJ (2003). High methionine and cholesterol diet abolishes endothelial relaxation. Arterioscler. Thromb. Vasc. Biol., 23, 1358-1363.
  • Widdop, R.E., Jones, E.S., Hannan, R.E. and Gaspari, T. (2003). Angiotensin AT2 receptor: cardiovascular friend or foe? (invited review). Brit. J. Pharmacol., in press.
  • Hannan RE, Davis EA & Widdop RE (2003). Functional role of angiotensin II AT2 receptor in modulation of AT1 receptor-mediated contraction in rat uterine artery: involvement of bradykinin and nitric oxide. Brit. J. Pharmacol., in press.