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Associate Professor Peter Molenaar

Faculty of Health,
School - Biomedical Sciences

Personal

Name
Associate Professor Peter Molenaar
Position(s)
Associate Professor
Faculty of Health,
School - Biomedical Sciences
IHBI Membership
Institute of Health Biomedical Innovation (IHBI),
IHBI Health Projects,
IHBI Biomedical Sciences - Tissue
Discipline *
Pharmacology and Pharmaceutical Sciences, Other Biological Sciences
Phone
+61 7 3138 8376
Fax
+61 7 3138 1534
Email
Location
View location details (QUT staff and student access only)
Qualifications

PhD (The University of Melbourne)

Professional memberships
and associations
  • Australian Society for Clinical and Experimental Pharmacology and Toxicology(ASCEPT)
  • British Pharmacological Society
Keywords

Beta-adrenoceptors, G-protein coupled receptors, Human Heart Research, in vitro human heart research

* Field of Research code, Australian and New Zealand Standard Research Classification (ANZSRC), 2008

Biography

Research theme: Health

Research discipline: Pharmacy

Research areas

Investigation of the molecular properties and physiological significance of different ‘states’ of the (1-adrenoceptor: (1-Adrenoceptors are proteins that exist in human heart which mediate the cardiostimulant effects of noradrenaline. Some (-blockers, such as (-)-CGP 12177 not only block the receptor but also stimulate it. To accommodate this finding we have proposed that noradrenaline and cardiostimulant (-blockers bind differently to the (1-adrenoceptor.

We are investigating: a. the specific features of the (1-adrenoceptor that are critical for activation of the receptor by (-blockers; b. whether activation of the receptor by (-blockers such as (-)-CGP 12177 causes progression of heart failure in an animal model of heart failure and; c. the chemical features of (-blockers that cause the receptor to be activated and not blocked. These studies are likely to lead to the improved design of (-blockers for clinical use.

The genetic basis of (-blocker responsiveness in human heart failure: The clinical effect of (-blockers in human heart failure is quite variable. Some patients show marked improvement in heart function whilst others show marginal or no improvement. In patients with non-ischemic cardiomyopathy treated with carvedilol we found that the Arg389Gly-(1-adrenoceptor polymorphism predicts improvement in left ventricular ejection fraction.

Investigation of phosphodiesterase enzymes that are responsible for the metabolism of cyclic AMP accumulated by activation of (1- and (2-adrenoceptors in human ventricle: In human heart phosphodisterase enzymes metabolize the cyclic AMP that is increased in response to activation of (-adrenoceptors. These enzymes can be considered to have a protective role against the harmful effects of excessive (-adrenoceptor activation. We are currently investigating the phosphodiesterases that are responsible for metabolism of cyclic AMP raised by activation of (1- and (2-adrenoceptors in human ventricle from patients with end-stage heart failure.

Areas of expertise:

  • Human heart research
  • G-protein coupled receptors
  • Beta-adrenoceptors
  • Polymorphisms

This information has been contributed by Associate Professor Peter Molenaar.

Teaching

Teaching discipline: Pharmacy

This information has been contributed by Associate Professor Peter Molenaar.

Publications

For more publications by this staff member, visit QUT ePrints, the University's research repository.