Key result
Angiotensinogen-deficient mice exhibited profound hypotension with a systolic blood pressure of 66.9 mm Hg compared to 100.4 mm Hg in wild-type mice.
Why the study?
Does angiotensinogen deficiency lower systolic blood pressure in mice?
Does angiotensinogen deficiency lower systolic blood pressure in mice?
Absolute Event Rate: 66.9% vs 100.4%
Angiotensinogen-deficient mice exhibit profound hypotension, demonstrating the indispensable role of the renin-angiotensin system in maintaining blood pressure.
Supports RAS essentiality for BP in mice; leaves open translation to human hypertension therapies.
The renin-angiotensin system is an enzymatic cascade that produces a potent vasoconstrictor octapeptide angiotensin II, through its physiologically inactive intermediate decapeptide angiotensin I, from their precursor angiotensinogen. In the present study, we generated angiotensinogen-deficient mice by homologous recombination in mouse embryonic stem cells. These mice do not produce angiotensinogen in the liver, resulting in the complete loss of plasma immunoreactive angiotensin I. The systolic blood pressure of the homozygous mutant mice was 66.9 +/- 4.1 mm Hg, significantly lower than that of wild-type mice (100.4 +/- 4.4 mm Hg). This profound hypotension in angiotensinogen-deficient mice demonstrates an indispensable role for the renin-angiotensin system in maintaining blood pressure.
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Tanimoto et al. (1994) studied Hypotension. Angiotensinogen deficiency (homozygous mutant) vs. Wild-type mice was evaluated on Systolic blood pressure. Angiotensinogen-deficient mice exhibited profound hypotension with a systolic blood pressure of 66.9 mm Hg compared to 100.4 mm Hg in wild-type mice.
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