What question did this study set out to answer?

To compare the effects of the angiotensin II type 1 receptor antagonists losartan, candesartan, and valsartan on platelet activation in stroke-prone spontaneously hypertensive rats.

April 1, 2001Journal of Cardiovascular Pharmacology

Inhibition of Platelet Activation in Stroke-Prone Spontaneously Hypertensive Rats: Comparison of Losartan, Candesartan, and Valsartan

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Population

Stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats

Comparison

Losartan, candesartan, or valsartan vs Untreated SHRSP and WKY rats

Design

Preclinical

Follow-up

14 days

Authors

AJAna JiménezCentro de Edafología y Biología Aplicada del Segura MMMercedes MontónHospital Universitario Fundación Jiménez Díaz RGRosa GarcíaHospital Universitario Virgen Macarena

Discussion

Member takes

Implication

Losartan may uniquely suppress platelet activation in hypertensive models; hypothesis-generating for differential ARB effects, requiring human confirmation.

Key Points

To compare the effects of the angiotensin II type 1 receptor antagonists losartan, candesartan, and valsartan on platelet activation in stroke-prone spontaneously hypertensive rats.
Administered losartan, valsartan, or candesartan (each at 20 mg/kg body weight per day for 14 days) to stroke-prone spontaneously hypertensive rats (SHRSP), comparing them to untreated SHRSP and normotensive Wistar-Kyoto (WKY) control rats.
Quantified platelet activation by measuring P-selectin expression via flow cytometry, analyzed ex vivo platelet adhesion to synthetic surfaces, and evaluated the binding of the radiolabeled thromboxane A2 agonist U46619.
Baseline platelet P-selectin expression was significantly higher in untreated SHRSP than in WKY controls (% P-selectin expression: SHRSP 15.5 +/- 0.8% [n = 8] vs. WKY 4 +/- 0.4%, p < 0.05).
Losartan reduced P-selectin expression to levels close to WKY controls and reduced ex vivo platelet adhesion, whereas P-selectin levels in SHRSP treated with valsartan or candesartan did not differ significantly from untreated SHRSP.
Losartan dose-dependently inhibited the binding of radiolabeled thromboxane A2 agonist U46619 to platelets ex vivo, demonstrating an antiplatelet effect through thromboxane receptor blockade independent of blood pressure lowering.

Structured PICO

Population

Stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats

Intervention

Losartan, candesartan, or valsartan (20 mg/kg body weight per day for 14 days)

Comparator

Untreated SHRSP and WKY rats

Outcome

Platelet activation assessed by P-selectin expression (flow cytometry) and ex vivo platelet adhesionsurrogate

Losartan uniquely reduces platelet activation in stroke-prone spontaneously hypertensive rats independently of blood pressure reduction, likely via TxA2-receptor blockade.

Cite This Study

Jiménez et al. (2001) studied this question.

synapsesocial.com/papers/6a7db953c2b228f3e18c9cc0 https://doi.org/10.1097/00005344-200104000-00007

Topics

Hypertension management

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Implication

Losartan may uniquely suppress platelet activation in hypertensive models; hypothesis-generating for differential ARB effects, requiring human confirmation.