Hormonal Pattern During Development of Hypertension in Spontaneously Hypertensive Rats (SHR)
- 1 January 1982
- journal article
- research article
- Published by Taylor & Francis in Clinical and Experimental Hypertension. Part A: Theory and Practice
- Vol. 4 (6), 915-935
- https://doi.org/10.3109/10641968209060762
Abstract
Urinary excretion of sodium, noradrenaline, dopa-mine, aldosterone, prostaglandin E2. and plasma renin activity were determined in 7 and 16 weeks old spontaneously hypertensive rats (SHR) and in two normotensive control strains, ordinary Wistar control rats (NCR) and Wistar-Kyoto normotensive rats (WKR). Each group consisted of 10–11 rats. The animals were kept in metabolic cages. Experiments were performed on standard diet (5–8 mmol Na+/100 g food) and with an increased (15.6 and 56.0 mmol Na+/100 g food) salt intake. At 7 weeks of age, when SHR are in a borderline phase of hypertension, they exhibited a decreased urinary sodium excretion, and an increased urinary noradrenaline excretion compared to controls. The latter might reflect an increased overall activity of the sympathetic nervous system. Urinary dopamine excretion was also increased probably mirroring a higher activity in a renal natriure-tic dopamine system. Plasma renin activity and urinary aldosterone excretion were depressed. At 16 weeks of age, when SHR are in an early established phase of hypertension, urinary sodium excretion was still lower in SHR, while urinary noradrenaline and dopamine excretions had become normal compared to controls. Plasma renin activity and urinary aldosterone excretion remained depressed. Urinary PGE2 excretion, only determined in this age group, was significantly higher in SHR. When sodium intake was increased 8-10 times the difference in urinary sodium excretion was diminished and not significantly lower in SHR. The salt load caused a doubling of the urinary dopamine excretion, while the noradrenaline excretion was unchanged. These findings might be compatible with the view that the decreased urinary sodium excretion in the young SHR would be caused by an increased sympathetic outflow to the kidneys promoting tubular sodium reabsorption while the increased urinary dopamine excretion is regarded as a compensatory mechanism to overcome the difficulties to excrete sufficient amounts of sodium.This publication has 19 references indexed in Scilit:
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