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January 1, 1998Hypertension Research19 citationsOpen Access

Effects of Renin-Angiotensin System Blockade and Dietary Salt Intake on Left Ventricular Hypertrophy in Dahl Salt-Sensitive Rats.

KSKoh‐ichi SugimotoTokyo Institute of TechnologyAFAkio FujimuraJichi Medical UniversityITIzumi TakasakiJuntendo University

Structured PICO

Does renin-angiotensin system blockade reduce blood pressure and left ventricular hypertrophy in Dahl salt-sensitive rats on high- or low-salt diets?

P
Population
12-week-old male Dahl salt-sensitive (DS) rats
I
Intervention
Angiotensin II receptor antagonist candesartan (3 mg/kg/d) or ACE inhibitor enalapril (30 mg/kg/d) under high-salt (8% NaCl) or low-salt (0.3% NaCl) diet
C
Comparator
Vehicle
O
Outcome
Blood pressure and left ventricular hypertrophy (left ventricular mass)surrogate

Sodium intake and hemodynamic load, rather than the renin-angiotensin system, appear to be the primary drivers of left ventricular hypertrophy in salt-sensitive hypertension.

Abstract

We studied the effects of chronic blockade of the renin-angiotensin system on hypertension and cardiac left ventricular hypertrophy (LVH) in Dahl salt-sensitive (DS) rats given a high-salt or low-salt diet. Experiment 1 Twelve-week-old male DS rats were fed an 8% NaCl diet and received the angiotensin II receptor (AT1) antagonist, candesartan (3 mg/kg/d), the angiotensin converting enzyme inhibitor enalapril (30 mg/kg/d), or vehicle for 6 wk after 3 wk of 8% salt-loading. Neither candesartan nor enalapril with concomitant high salt-loading attenuated the blood pressure (BP) elevation. LVH was also not attenuated significantly by these treatments. Experiment 2 After 8 wk of 8% salt-loading, the rats were given a 0.3% NaCl diet and concurrently received candesartan, enalapril, or vehicle for 5 wk. Switching from the high-salt to low-salt diet significantly decreased BP and left ventricular mass in the vehicle-treated animals. Both candesartan and enalapril normalized BP during salt-depletion; the blockade of the renin-angiotensin system produced an additive reduction in LVH. These findings suggest that sodium intake and hemodynamic load, but not the renin-angiotensin system, may be major determinants of the development of LVH in DS rats.

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Cite This Study

Sugimoto et al. (1998) studied this question.

synapsesocial.com/papers/6a20bf956aba112f1d33799ahttps://doi.org/10.1291/hypres.21.163
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cardiac Hypertrophy and the Blockade of Angiotensin II Receptors by Losartan in Salt-Loaded Dahl Salt-Sensitive Rats.1994 · 5 citations
  2. 2Reduction of development of left ventricular hypertrophy in salt-loaded Dahl salt-sensitive rats by angiotensin II receptor inhibition1996 · 32 citations
  3. 3Cardiac hypertrophy and cardiac renin–angiotensin system in Dahl rats on high salt intake2000 · 36 citations
  4. 4Angiotensin Blockade Prevents Salt-Induced Injury of the Renal Circulation in Spontaneously Hypertensive Rats2009 · 29 citations
  5. 5Prevention of salt induced hypertension and fibrosis by angiotensin converting enzyme inhibitors in Dahl S rats2007 · 34 citations