Key result
AT1b receptor deficiency diminished Angiotensin II-induced contractility in the infra-renal aorta but had no effect on Angiotensin II-induced atherosclerosis or aortic aneurysms.
Why the study?
Does AT1b receptor deficiency prevent AngII-induced atherosclerosis and aortic aneurysms in hypercholesterolemic mice?
Does AT1b receptor deficiency prevent AngII-induced atherosclerosis and aortic aneurysms in hypercholesterolemic mice?
While AT1b receptors mediate AngII-induced contractility in the infra-renal aorta, they do not play a significant role in the development of AngII-induced atherosclerosis or aortic aneurysms in mice.
AT1b deficiency does not prevent AngII-induced atherosclerosis or aneurysms in mice; leaves open receptor-specific roles in human vascular disease.
Background: Angiotensin II (AngII), the main bioactive peptide of the renin angiotensin system, exerts most of its biological actions through stimulation of AngII type 1 (AT1) receptors. This receptor is expressed as 2 structurally similar subtypes in rodents, termed AT1a and AT1b. Although AT1a receptors have been studied comprehensively, roles of AT1b receptors in the aorta have not been defined.
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Poduri et al. (2012) studied Angiotensin II-induced atherosclerosis and aortic aneurysms (n=26). AT1b receptor deficiency vs. AT1b receptor +/+ (wild type) was evaluated on Atherosclerotic lesion area and supra-renal aortic luminal diameter. AT1b receptor deficiency diminished Angiotensin II-induced contractility in the infra-renal aorta but had no effect on Angiotensin II-induced atherosclerosis or aortic aneurysms.
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