Effects of altered dietary sodium intake on hormonal profiles in salt-sensitive hypertensive rats

in Journal of Endocrinology
Authors:
N. Hazon
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I. W. Henderson
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ABSTRACT

Blood pressure and selected putatively influential hormones were measured in Brattleboro rats which were without diabetes insipidus and which were subjected to various manipulations in dietary sodium intake. Rats fed a control diet from weaning to 16 weeks of age showed a slow increase in blood pressure whereas rats fed a sodium-enriched diet for the same period exhibited sustained hypertension (115±3 versus 169±5 (s.e.m.) mmHg). In animals fed a sodium-enriched diet plasma concentrations of antidiuretic hormone (ADH) were significantly increased from 55±8 to 108±5 fmol/l. Rats fed the control diet from weaning (group A) and subsequently maintained on that diet or changed to a sodium-enriched diet or sodium-deficient diet showed no differences in their blood pressure. Plasma hormone concentrations were similar in these groups, with the exception of aldosterone suppression in rats switched from control to a sodium-enriched diet (0·26±0·04 versus 0·08±0·03 nmol/l; P <0·001). Animals fed the sodium-enriched diet from weaning to 16 weeks of age (group b) and either maintained on that diet or changed to a control diet showed little change in their established hypertension. Transfer to the control diet was associated with increased plasma renin concentrations (PRC) (13·8±2·1 to 122·6±6·2 nmol/l) and plasma aldosterone concentrations (0·04±0·01 to 0·08±0·01 nmol/l; P<0·001) but corticosteroids and ADH concentrations were unchanged. Rats maintained on the sodium-enriched diet from weaning to 16 weeks of age and transfered to a sodium-deficient diet exhibited increases in their established hypertensive blood pressures (maximally 205±4 versus 170±4 mmHg) together with significant increases in PRC (13·8 ±2·1 to 297±79 nmol/l; P< 0·001), aldosterone (0·04±0·01 to 0·23±0·07 nmol/l; P <0·001) and ADH (82·9±15·5 to 466±118 fmol/l; P <0·001), although plasma concentrations of corticosteroids were again unaffected. Thus it would appear that there is a critical developmental stage at which exposure to a sodium-enriched diet subsequently leads to hypertension. Abrupt withdrawal of the sodium-enriched diet produces an exaggerated hypertension involving changes in both ADH and the renin-angiotensin-aldosterone system.

Journal of Endocrinology (1990) 127, 243–248

 

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