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November 1, 2000American Journal of HypertensionOpen Access

Effects of the AT1 receptor antagonist on adhesion molecule expression in leukocytes and brain microvessels of stroke-prone spontaneously hypertensive rats

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Why the study?

Does AT1 receptor antagonism or ACE inhibition reduce adhesion molecule expression in stroke-prone spontaneously hypertensive rats?

Population

Male stroke-prone spontaneously hypertensive rats (SHRSP) at 19 weeks of age

Comparison

AT1 receptor antagonist or ACEI administered for… vs Control SHRSP and age-matched Wistar-Kyoto rats

Design

Preclinical

Follow-up

4 weeks

Authors

KTKumiko TakemoriHIHiroyuki ItoTSTakayoshi Suzuki

Discussion

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Overview

AT1 antagonism may reduce adhesion molecules in hypertensive models; leaves open clinical relevance or superiority over ACEIs in humans.

Structured PICO

Does AT1 receptor antagonism or ACE inhibition reduce adhesion molecule expression in stroke-prone spontaneously hypertensive rats?

P
Population
Male stroke-prone spontaneously hypertensive rats (SHRSP) at 19 weeks of age
I
Intervention
AT1 receptor antagonist (TCV-116, 0.5 mg/kg/day) or ACEI (captopril, 20 mg/kg/day) administered for 4 weeks
C
Comparator
Control SHRSP (untreated) and age-matched Wistar-Kyoto rats (WKY)
O
Outcome
Expression of Mac-1 in leukocytes and ICAM-1, AT1 receptor, and GLUT-1 in endothelial cellssurrogate

AT1 receptor antagonism and ACE inhibition ameliorate the enhanced expression of adhesion molecules in stroke-prone spontaneously hypertensive rats, highlighting the role of angiotensin II in hypertensive microvascular injury.

Cite This Study

Takemori et al. (2000) studied this question.

synapsesocial.com/papers/6a815f702bdcf510039cd7f5https://doi.org/10.1016/s0895-7061(00)01202-4
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