Key result
Mice with a selective mutation in the PKGI alpha leucine zipper domain developed significant, sustained elevations in systolic blood pressure (143 vs 113 mmHg) despite normal renal function.
Population
Mice with a selective mutation in the N-terminal protein interaction domain of PKGIalpha
Design
Preclinical
Authors
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Suggests a primary vascular smooth muscle mechanism for hypertension in mice; leaves open relevance to human disease and clinical translation.
Mean Difference: 30
Absolute Event Rate: 143% vs 113%
p-value: p=<0.01
High blood pressure can arise from a primary abnormality of vascular smooth muscle cell contractile regulation via PKGIalpha, independent of primary renal abnormalities.
Michael et al. (2008) studied Hypertension. PKGI alpha leucine zipper mutation (LZM) vs. Wild-type (WT) mice was evaluated on Systolic blood pressure (mmHg) (Mean difference 30 mmHg, p=<0.01). Mice with a selective mutation in the PKGI alpha leucine zipper domain developed significant, sustained elevations in systolic blood pressure (143 vs 113 mmHg) despite normal renal function.
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