Key result
ATRAP deficiency in mice exacerbated angiotensin II-mediated hypertension and increased positive sodium balance via enhanced ENaC stimulation in an aldosterone-independent manner.
Why the study?
Does ATRAP deficiency exacerbate angiotensin II-mediated hypertension and sodium retention in mice?
Does ATRAP deficiency exacerbate angiotensin II-mediated hypertension and sodium retention in mice?
ATRAP deficiency exacerbates angiotensin II-mediated hypertension by enhancing renal sodium retention via ENaC stimulation in an aldosterone-independent manner.
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ATRAP disruption may alter BP responses to stimuli; leaves open clinical translation to human hypertension.
Ohsawa et al. (2014) studied Angiotensin II-induced hypertension. ATRAP deficiency (gene-targeted disruption) vs. Wild-type mice was evaluated on Blood pressure and positive sodium balance. ATRAP deficiency in mice exacerbated angiotensin II-mediated hypertension and increased positive sodium balance via enhanced ENaC stimulation in an aldosterone-independent manner.
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