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Title: The renin angiotensin aldosterone axis : relationships with other hormone systems, and novel applications for angiotensin converting enzyme inhibitors
Author: Lee, Alison Frances Clare
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2000
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The aim of this thesis was to look at the renin angiotensin system both in clinical heart failure, and in relation to other physiological systems where an interaction may exist. Furthermore, to address new areas where a potential for benefit with Angiotensin Converting Enzyme (ACE) inhibitors might occur. To this end there are five studies discussed within the thesis. It is shown that in a group of heart failure patients, stabilised on maximum tolerated dose of ACE inhibitor, mean levels of plasma neurohormones were remarkably stable over 18 months. Reactivation of aldosterone occurred in 13/97 samples (13.5%) in 5/22 (23%) individuals, and reactivation of angiotensin II occurred in 8/102 samples (8%), in 6/22 (27%) individuals. These appear to be sporadic phenomenon, and contrary to previous dogma, they do not herald disease progression. Using endothelial function as a surrogate marker for cardiovascular events in hyperlipidaemic patients, it is shown that interruption of the renin angiotensin system using ACE inhibition, causes increases in both endothelial dependent and endothelial independent vasodilation. This could lead to the use of ACE inhibitors in hyperlipidaemic patients to reduce cardiovascular events, over and above traditional therapy such as statins. Subsequent to the above, the effect of lisinopril on nitrate/nitrite excretion as a marker of nitric oxide metabolism in hypercholesterolaemia was assessed. The levels of plasma nitrate/nitrite after an eighteen hour fast in twenty of the hyperlipidaemic volunteers were taken, and contrasted with values in normal volunteers. Lisinopril was found to have no effect on nitrate/nitrite levels in the hyperlipidaemic patients. Evidence in the literature has suggested interactions between the renin angiotensin system, and oestradiol, whose mechanism of vasodilation is still under debate. This study, using forearm plethysmography, looked at whether vasodilation by ovarian hormones was due to effects on the renin angiotensin system. No evidence was found that either oestradiol, or medroxy-progesterone affected vascular responses to angiotensin II, or altered the activity of vascular ACE activity.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available