March 5, 2001Clinical and Experimental Pharmacology and PhysiologyOpen Access

KRH‐594, A New Angiotensin At1 Receptor Antagonist, Prevents End‐Organ Damage In Stroke‐Prone Spontaneously Hypertensive/Izm Rats

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Why the study?

Does KRH-594 prevent end-organ damage and improve survival in salt-loaded stroke-prone spontaneously hypertensive rats?

Population

salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP/Izm)

Design

Preclinical

Follow-up

11 weeks

Authors

YIYoichi InadaMatsumoto University STShigeki TazawaKissei Pharmaceutical (Japan)MMMakoto MurakamiJapan Agency for Medical Research and Development

Discussion

Member takes

Implication

Does not inform clinical practice; leaves open translation of KRH-594 benefits to human hypertensive disease.

Structured PICO

Does KRH-594 prevent end-organ damage and improve survival in salt-loaded stroke-prone spontaneously hypertensive rats?

Population

salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP/Izm)

Intervention

KRH-594 (angiotensin AT1 receptor antagonist) 3 and 10 mg/kg per day orally for 11 weeks

Outcome

progression of renal failure, end-organ damage, and survival rate

KRH-594, a novel AT1 receptor antagonist, demonstrates protective effects against hypertensive end-organ damage and mortality in a preclinical rat model.

Cite This Study

Inada et al. (2001) studied this question.

synapsesocial.com/papers/6a703e6d6c240de38cdbbae3 https://doi.org/10.1046/j.1440-1681.2001.03430.x

Topics

Hypertension management

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KRH‐594, A New Angiotensin At1 Receptor Antagonist, Prevents End‐Organ Damage In Stroke‐Prone Spontaneously Hypertensive/Izm Rats

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

KRH‐594, A New Angiotensin At1 Receptor Antagonist, Prevents End‐Organ Damage In Stroke‐Prone Spontaneously Hypertensive/Izm Rats

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

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