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January 1, 1995Journal of Hypertension

Role of angiotensin II in cerebrovascular and renal damage in deoxycorticosterone acetate-salt hypertensive rats

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Population

Deoxycorticosterone acetate-salt hypertensive rats

Comparison

TCV-116 or enalapril given orally once a day… vs Untreated DOCA-salt hypertensive rats and…

Design

Preclinical

Follow-up

3 weeks

Authors

TWTakeo WadaUniversity of BaselRKRei KanagawaTakeda (Japan)YIYoshimasa IshimuraHiroshima University

Discussion

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Implication

Does not inform clinical practice; extends experimental evidence for BP-independent RAS blockade in salt-sensitive hypertension models.

Key Points

  • To evaluate how blocking the renin-angiotensin system with an angiotensin II receptor antagonist or an ACE inhibitor affects hypertension and end-organ damage in DOCA-salt hypertensive rats.
  • DOCA-salt hypertensive rats were established via uninephrectomy, DOCA pellet implantation, and 1% NaCl loading.
  • Rats received daily oral treatments of the angiotensin II receptor antagonist TCV-116 (0.1 or 1 mg/kg) or the ACE inhibitor enalapril (10 mg/kg) from weeks 3 to 6 post-surgery.
  • Measured endpoints included blood pressure, body weight, plasma renin, plasma creatinine, blood urea nitrogen, urinary protein, brain oedema, and cortical omega 3-subtype benzodiazepine receptor binding.
  • By week 3, DOCA-salt rats developed severe hypertension (~200 mmHg) with suppressed plasma renin; by week 6, renin rose slightly above normal alongside weight loss, proteinuria, elevated blood urea nitrogen, plasma creatinine, and brain oedema.
  • Treatment with either TCV-116 or enalapril prevented renal damage and weight loss with negligible effects on blood pressure levels.
  • Enalapril prevented brain oedema and the rise in cortical benzodiazepine binding, while high-dose TCV-116 (1 mg/kg) markedly suppressed both cerebral markers.

Structured PICO

P
Population
Deoxycorticosterone acetate (DOCA)-salt hypertensive rats (produced by uninephrectomy, implantation with DOCA pellets and 1% NaCl loading)
I
Intervention
TCV-116 (0.1 or 1 mg/kg) or enalapril (10 mg/kg) given orally once a day from 3 to 6 weeks after the operation
C
Comparator
Untreated DOCA-salt hypertensive rats and sham-operated rats
O
Outcome
Development of hypertension and end-organ damage (body weight, blood pressure, plasma renin and creatinine, urinary protein, blood urea nitrogen, brain oedema, and omega 3-subtype benzodiazepine receptor binding in the brain)surrogate

In DOCA-salt hypertensive rats, cerebral and renal damage is associated with renin-angiotensin system activity and can be prevented by ACE inhibitors or ARBs independently of blood pressure reduction.

Cite This Study

Wada et al. (1995) studied this question.

synapsesocial.com/papers/6a758c3a1cd7cac2185ffc47https://doi.org/10.1097/00004872-199501000-00017

Topics

Hypertension management
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Also Consider

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

  1. 1Role of angiotensin II in renal injury of deoxycorticosterone acetate-salt hypertensive rats.1994 · 117 citations
  2. 2Effects of Angiotensin-Converting Enzyme Inhibitor and Angiotensin Type 1 Receptor Antagonist in Deoxycorticosterone Acetate–Salt Hypertensive Mice Lacking <i>Ren-2 Gene</i>2001 · 42 citations
  3. 3Blockade of Angiotensin Receptors in the Anterior Hypothalamic Preoptic Area Lowers Blood Pressure in DOCA-Salt Hypertensive Rats.2000 · 50 citations
  4. 4Central renin-angiotensin system and the pathogenesis of DOCA-salt hypertension in rats1986 · 85 citations
  5. 5Different Contributions of Endothelin-A and Endothelin-B Receptors in the Pathogenesis of Deoxycorticosterone Acetate–Salt–Induced Hypertension in Rats1999 · 114 citations