Angiotensin II/AT2 receptor-induced vasodilation in stroke-prone spontaneously hypertensive rats involves nitric oxide and cGMP-dependent protein kinase

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Population

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

Comparison

Valsartan for 14 days, followed by Angiotensin… vs Wistar-Kyoto (WKY) rats and/or absence of L-NAME

Design

Preclinical

Follow-up

14 days

Authors

Discussion

Does not support practice change; leaves open whether AT2R-NO enhancement by AT1R blockade translates to human hypertension.

Population

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

Intervention

Valsartan for 14 days, followed by Angiotensin II with or without N-nitro-L-arginine methyl ester (L-NAME)

Comparator

Wistar-Kyoto (WKY) rats and/or absence of L-NAME

Outcome

Vasodilation response to Angiotensin II, eNOS expression, NO concentration, cGKI expression, and NAD(P)H oxidase activitysurrogate

Chronic AT1R antagonism with valsartan enhances AT2R-mediated vasodilation via NO/cGMP pathways and cGKI upregulation in a hypertensive rat model.

Savoia et al. (2006) studied this question.

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