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The effects of oestrogen on renal and systemic haemodynamics in the rat: influence of intrarenal vasoactive substances and plasma volume status

Evans, John Kenrick

The effects of oestrogen on renal and systemic haemodynamics in the rat: influence of intrarenal vasoactive substances and plasma volume status Thumbnail


Authors

John Kenrick Evans



Abstract

The effects of oestrogen on renal and systemic haemodynamics, intrarenal vasoactive substances and plasma volume status have been studied in adult female normotensive and spontaneously hypertensive rats.
Administration of oestrogen to both strains of rat resulted in a reduction in renal blood flow, due to an increased renal vascular resistance in the presence of an increase in both plasma renin substrate concentration and activity.
In the normotenaive rat, oestrogen affected a rise in arterial pressure, accompanied by an expanded plasma volume, and either an unchanged or increased plasma renin activity. Whilst changes in arterial pressure were reciprocally related to changes in plasma volume, no relationship was noted between arterial pressure and plasma renin activity. In the spontaneously hypertensive rat, oestrogen caused a fall in arterial pressure, due to a reduced peripheral vascular resistance.
The oestrogen-induced reduction in renal perfusion was due to enhanced local, intrarenal generation of angiotensin II - as evidenced by an increase in renal perfusion in both strains of oestrogen treated rat after angiotensin converting enzyme inhibition (captopril). Evidence from studies involving prostaglandin synthesis inhibition (indomethacin), plasma prorenin activation (trypsin) and saralasin treatment (angiotensin II blockade)indicate that a proportion of this angiotensin II-mediated intrarenal vasoconstriction involved at least a prostaglandin-dependant pathway, in addition to an alteration in intrarenal vascular angiotensin II receptor density. The oestrogen-induced rise in arterial pressure was determined principally by plasma volume expansion, although angiotensin II also contributed to this rise - as demonstrated by a lessening of oestrogen-induced hypertension by captopril. The oestrogen-induced fall in arterial pressure appeared to be prostaglandin-dependant, although indomethacin failed to influence arterial pressure in oestrogen treated epcntaneously hypertensive rats.
This investigation demonstrates that an alteration in the normal equilibrium between intrarenal vasoactive substances can, in conjunction with a change in plasma volume status, lead to disturbances in both renal and systemic haemodynamics during oestrogen treatment.

Publicly Available Date Mar 29, 2024

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