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Abstract

In this thesis I examined vascular physiology, with an emphasis on venous
physiology, of two important neuro-hormones, aldosterone and bradykinin, in health
and in chronic heart failure. Capacitance venous tone governs the volume of blood in
the peripheral vs. central circulation and thus indirectly influences cardiac output.
Mechanisms that control venous tone in health and in heart failure are poorly
understood.
Chapter 1 discusses the importance of venous physiology in governing cardiac output
in health and heart failure. The significance of pressure volume relationships, rather
than pressure flow relationships in capacitance veins is explained. The physiological
measures and the terms used to describing changes in parameters are defined.
Chapter 2 is a literature review of pharmacology and physiology of aldosterone and
bradykinin, with an emphasis on vascular physiology in health and in chronic heart
failure.
Chapter 3 describes in detail our methods of assessing both resistance and capacitance
vascular functions. It examines changes to vasculature with a semi-supine posture,
relationship between arterial flow and venous capacitance, and compares two
established techniques in assessing capacitance veins.
Chapter 4, 5 and 6 examines in detail the effects of aldosterone and bradykinin on
human forearm vasculature, and differences in vascular responses between states of
health and heart failure are discussed.
The important new findings of this thesis are:
1. In physiological concentrations, aldosterone does not acutely alter vascular
physiology in health. 2. In contrast, in treated heart failure aldosterone decreases blood flow in
resistance vessels but not in capacitance vessels
3. Bradylcinin modulates venous capacitance in health via its Type 2 receptor.
However, bradykinin does not contribute to basal vascular tone in health
4. In angiotensin-converting-enzyme-inhibitor-treated heart failure, bradykinin
contributes to basal venous tone. In contrast, bradykinin does not contribute to
venous tone in heart failure treated with angiotensin II receptor antagonists.
5. In mild to moderate heart failure bradykinin effects are mediated via the Type
2 Bradykinin receptor.
6. A paradoxical enhanced venodilatation was discovered in heart failure patients
on both aspirin and angiotensin converting enzyme inhibitors, in comparison
to those only on the latter.

Item Type:	Thesis - PhD
Authors/Creators:	Gunaruwan, Thevarathanthirige Punsiri Prasad
Keywords:	Cardiovascular system, Heart failure, Aldosterone, Bradykinin
Copyright Holders:	The Author
Copyright Information:	Copyright 2008 the Author - The University is continuing to endeavour to trace the copyright owner(s) and in the meantime this item has been reproduced here in good faith. We would be pleased to hear from the copyright owner(s).
Additional Information:	Thesis (PhD)--University of Tasmania, 2008. Includes bibliographical references
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