Key result
Angiotensin type 1 receptor deletion in mice resulted in larger baseline afferent (19.5 vs 13.9 microm) and efferent (15.5 vs 10.8 microm) arterioles and absent responses to ANG II.
Why the study?
Does angiotensin type 1 receptor deletion alter renal microvascular reactivity to vasoconstrictors and vasodilators in mice?
Population
Angiotensin type 1A (AT(1A)) and 1B (AT(1B)) receptor double knockout (AT1DKO) mice and wild-type (WT) mice
Comparison
In vitro blood perfused juxtamedullary nephron… vs Wild-type (WT) mice
Design
Preclinical
Authors
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No immediate clinical implications; leaves open whether AT1 receptor mechanisms translate to human renal microvascular disease.
Does angiotensin type 1 receptor deletion alter renal microvascular reactivity to vasoconstrictors and vasodilators in mice?
Angiotensin II signaling via the AT1 receptor is essential for maintaining basal renal microvascular tone and normal reactivity to vasoconstrictors and vasodilators.
Park et al. (2007) studied Renal microvascular disease. Angiotensin type 1A and 1B receptor deletion (AT1DKO) vs. Wild-type (WT) mice was evaluated on Baseline diameters of afferent and efferent arterioles and responses to ANG II, NE, and ACh. Angiotensin type 1 receptor deletion in mice resulted in larger baseline afferent (19.5 vs 13.9 microm) and efferent (15.5 vs 10.8 microm) arterioles and absent responses to ANG II.
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