Key result
High sodium diet increased blood pressure and low sodium diet with furosemide decreased blood pressure without altering angiotensin II levels in Ren-2 transgenic rats.
Why the study?
Does dietary salt load or depletion alter blood pressure and angiotensin II levels in male and female Ren-2 transgenic rats?
Does dietary salt load or depletion alter blood pressure and angiotensin II levels in male and female Ren-2 transgenic rats?
Sex differences in salt-sensitive hypertension appear more pronounced in female Ren-2 rats; leaves open translation to human disease.
BACKGROUND: In the present study we evaluated plasma and kidney angiotensin II (ANG II) levels in female and male Ren-2 transgenic rats (TGR) in comparison to age-matched female and male normotensive Hannover Sprague-Dawley rats. METHODS: The rats were maintained on a normal sodium (NS) diet (0.6% NaCl) or fed a high sodium (HS) diet (2% NaCl) for 4 days or were sodium depleted by administration of 40 mg furosemide per liter drinking water overnight followed by 3 days of low sodium diet (0.01% NaCl) (LS + F). ANG II levels were determined by radioimmunoassay. RESULTS: Female TGR at the age of 38 days were already hypertensive and had developed cardiac hypertrophy, whereas male TGR at this age still exhibited a normotensive phenotype. HS diet increased the blood pressure (BP) but did not alter the ANG II levels in TGR at any age. LS + F decreased the BP without significant change in ANG II concentrations in TGR. Female TGR responded to salt loading and salt depletion by more pronounced changes in BP than male TGR. CONCLUSIONS: Female TGR develop hypertension more rapidly and the salt-sensitive component of hypertension is more pronounced in female than in male TGR.
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Husková et al. (2007) studied Hypertension. High sodium diet or low sodium diet with furosemide vs. Normal sodium diet (0.6% NaCl) was evaluated on Blood pressure and angiotensin II levels. High sodium diet increased blood pressure and low sodium diet with furosemide decreased blood pressure without altering angiotensin II levels in Ren-2 transgenic rats.
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