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Studies of the mechanisms involved in the control of the renal excretion of sodium

Studies of the mechanisms involved in the control of the renal excretion of sodium
Studies of the mechanisms involved in the control of the renal excretion of sodium

The urinary excretion of sodium is known to be sensitive to changes in the renal blood flow and to lie dependent upon localised functions within the kidney. It line also been suggested that changes in the blood flow to specific regions of the kidney may be important in the renal control of sodium balance. This thesis describes an experimental investigation into these concepts using the laboratory rat. Experimental methods were developed for studying the blood flow distribution within the kidney of the rat. The sodium retaining hormone angiotensin TT was found to cause sodium retention at low doses and sodium excretion at high closes.The sodium retention occurred simultaneously with reduced blood flows to all regions of the kidney. This sodium retention does not require the synthesis of renal protein since it was not inhibited by cycloheximide, but it may require renal vasoconstriction. ISarcosine-1, L.eucine-8]-nngiotensin II had no vasoconstrictor properties and did not cause sodium, retention but inhibited the vasoconstrictor and sodium retaining actions of angiotensin TI. The sodium excretion caused by high probably unphysiological, doses of angiotensin IT occurred simultaneously with increased blood flows to the inner regions of the kidney. Long-term alterations in dietary sodium intake were studied. Sodium depletion caused renal sodium retention, and sodium loading caused renal sodium excretion. The blocd flows to all regions of the kidney were reduced by sodium depletion, and increased by sodium loading(no redistribution of blood flow within the kidney was observed. The role of angiotensin II in the control of sodium balance, and mechanism of angiotensin II action on the kidney is discussed.

University of Southampton
Cambridge, David
Cambridge, David

Cambridge, David (1977) Studies of the mechanisms involved in the control of the renal excretion of sodium. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

The urinary excretion of sodium is known to be sensitive to changes in the renal blood flow and to lie dependent upon localised functions within the kidney. It line also been suggested that changes in the blood flow to specific regions of the kidney may be important in the renal control of sodium balance. This thesis describes an experimental investigation into these concepts using the laboratory rat. Experimental methods were developed for studying the blood flow distribution within the kidney of the rat. The sodium retaining hormone angiotensin TT was found to cause sodium retention at low doses and sodium excretion at high closes.The sodium retention occurred simultaneously with reduced blood flows to all regions of the kidney. This sodium retention does not require the synthesis of renal protein since it was not inhibited by cycloheximide, but it may require renal vasoconstriction. ISarcosine-1, L.eucine-8]-nngiotensin II had no vasoconstrictor properties and did not cause sodium, retention but inhibited the vasoconstrictor and sodium retaining actions of angiotensin TI. The sodium excretion caused by high probably unphysiological, doses of angiotensin IT occurred simultaneously with increased blood flows to the inner regions of the kidney. Long-term alterations in dietary sodium intake were studied. Sodium depletion caused renal sodium retention, and sodium loading caused renal sodium excretion. The blocd flows to all regions of the kidney were reduced by sodium depletion, and increased by sodium loading(no redistribution of blood flow within the kidney was observed. The role of angiotensin II in the control of sodium balance, and mechanism of angiotensin II action on the kidney is discussed.

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Published date: 1977

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Local EPrints ID: 459734
URI: http://eprints.soton.ac.uk/id/eprint/459734
PURE UUID: 44b6e911-1923-4c30-8a30-90c09ee7a768

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Date deposited: 04 Jul 2022 17:17
Last modified: 04 Jul 2022 17:17

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Author: David Cambridge

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