Key result
Angiotensin II infusion in female rats significantly increased morphological deformities in the coronary resistance artery network compared to controls (74 vs 13 deformities; p<0.01).
Why the study?
Although segmental remodeling and rarefaction by Angiotensin II and hypertension are established, less is known about alterations in resistance artery network geometry potentially induced by them.
Chronic Angiotensin II infusion in female rats induces significant morphological remodeling and deformities in the intramural coronary resistance artery network, which likely contributes to elevated vascular resistance.
May inform mechanisms of female coronary remodeling; leaves open human translation and requires clinical validation.
Segmental remodeling of resistance arteries, inhibition of angiogenetic processes, their rarefaction by AngiotensinII and hypertension are accepted facts. Less is known about alterations in resistance artery network geometry potentially induced by them. Female rats were infused with 100 ng/kg/min AngiotensinII with osmotic minipumps for four weeks that raised mean arterial blood pressure from 98 ± 3 to 125 ± 7 mmHg. Geometry of the left coronary artery system was studied on plastic casts and on in situ microsurgically prepared, saline infused video-microscoped networks (n = 13 and 11 controls and hypertensives, respectively). Parallel running branches, broken course of larger branches, multiple branchings and branch crossings have been identified (13 and 74 such deformities, in control and hypertensive networks, respectively, p < 0.01). Bifurcation angles increased with increasing asymmetry of daughter branches but not in hypertensives. Dividing the whole network (theoretically) into several hundreds of 50μm long ring units, ring frequency peaked at 200μm diameter in normal networks. This peak diminished and was replaced by a peak at 300μm in hypertensives (p < 0.01). In controls, diameter of vascular units decreased at a fairly even rate with flow distance from the orifice. The 350, 200, 150μm diameter units were found with highest frequencies at flow distances around 2.5, 5.5 and 7.5mm, respectively. This regular pattern disintegrated in hypertensives. Higher blood flow routes were needed to cover the same distance from the orifice (p < 0.01). Shrinkage and diminishment of many parallel connected 200μm segments, concomitant enlargement of many larger segments accompanied with morphological deformities can be expected to contribute to elevated vascular resistance.
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Monori-Kiss et al. (2020) studied Hypertension (n=24). Angiotensin II vs. Control was evaluated on Morphological deformities in the coronary resistance artery network (p=<0.01). Angiotensin II infusion in female rats significantly increased morphological deformities in the coronary resistance artery network compared to controls (74 vs 13 deformities; p<0.01).
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