Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.776309
Title: Circulatory effects of renal extracts in the rat and rabbit
Author: McKechnie, Kenneth C. W.
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1982
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Abstract:
The initial aim of this project was to study a new pressor substance of renal origin called renopressin, which was independent of the renin-angiotensin system. I was unable to obtain any evidence of the existence of this factor. The second and major project was to investigate the antihypertensive action of a lipid extract of the kidney. 1. The lipid was an alkyl ether analogue of phosphatidylcholine (AEPC). Rats were made hypertensive by placing a clip on one renal artery and removing the contralateral kidney. After six weeks arterial and venous catheters were implanted and blood pressure as recorded. Multiple injections of AEPC were then given to the rats. There was a short lasting fall in blood pressure but no long term antihypertensive activity was present. The possible reasons for this lack of long term antihypertensive activity are discussed. 2. The estimation of cardiac output in anaesthetised rats by thermodilution was validated against isotope dilution. 3. The haemodynamic action of AEPC in anaesthetised and conscious rats was examined. AEPC was found to cause no change in cardiac output but caused a fall in total peripheral resistance (TPR). The fall in TPR was due to a general vasodilation throughout the systemic circulation. 4. The effect of AEPC on pressor responses to noradrenaline and angiotensin II were examined. AEPC was found to attenuate the pressor responses of both agents. It was not possible to block pharmacologically the vasodepressor action of AEPC using antagonists to P-adrenergic and muscarinic agents, to histamine and to prostaglandin synthesis. 5. AEPC was found to cause a vasodepressor effect in isolated perfused mesentery when contractions were induced by noradrenaline but not when contractions were caused by high-K+ Krebs, AEPC had no effect on tonic or phasic activity in isolated portal vein. It is suggested that AEPC may act directly on vascular smooth muscle and block transmembrane calcium fluxes through receptor operated calcium channels.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.776309  DOI: Not available
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