Arterial function, physiological stress and the role of nitric oxide

Campbell, Ross I. 2008. Arterial function, physiological stress and the role of nitric oxide. PhD Thesis, Cardiff University.

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Abstract

Cardiovascular disease is the leading cause of death in the western world. Hypertension is a major risk factor for cardiovascular diseases and blood pressure is in turn markedly influenced by large artery stiffness. Recently a number of studies have reported that apparently healthy normotensive individuals who exhibit an exaggerated systolic blood pressure response on exercise are at increased risk of developing subsequent sustained hypertension and cardiovascular disease. It is likely that an exaggerated systolic blood pressure response on exercise represents an abnormal response of the large artery during dynamic exercise. In this thesis the normal responses of large arteries to different types and intensities of exercise was investigated in healthy normotensive subjects. Whilst distensibility of limb conduit arteries was measured for up to 15 minutes following exercise aortic distensibility did not change. An exaggerated systolic blood pressure response on exercise was not observed in healthy subjects without other conventional cardiovascular risk factors, but was observed frequently in the presence of such risk factors. Subjects with an exaggerated systolic blood pressure response on exercise did not show increased limb conduit artery distensibility immediately following exercise (and by implication during exercise). Blockade of NO synthesis prevented the increase in limb conduit artery distensibility seen in the first few minutes following exercise, but did not abrogate the more sustained increase in arterial distensibility following exercise. Systemic blockade of NO synthesis caused marked changes in systemic haemodynamics at risk, but these were markedly attenuated during exercise. The impact of mental stress on arterial function was also assessed. Whilst peripheral microvessels vasodilated, large arteries stiffened and this largely accounted for the observed increase in blood pressure.

Item Type:	Thesis (PhD)
Status:	Unpublished
Schools:	Medicine
Subjects:	R Medicine > R Medicine (General)
ISBN:	9781303224478
Funders:	British Heart Foundation
Date of First Compliant Deposit:	30 March 2016
Last Modified:	16 Jul 2018 11:31
URI:	https://orca.cardiff.ac.uk/id/eprint/55170

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