Key result
Hypertension impairs acetylcholine-induced mesenteric vasorelaxation despite increased eNOS activation in stroke-prone rats.
Why the study?
The mechanism underlying mesenteric artery vasorelaxation and endothelial dysfunction in stroke-prone spontaneously hypertensive rats was unclear.
Population
Second-order mesenteric arteries from stroke-prone spontaneously hypertensive rats and Wistar-Kyoto controls
Comparison
Acetylcholine concentration-response with or without NO synthase and indomethacin inhibition
Design
Preclinical experimental study
Authors
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May indicate compensatory eNOS in hypertensive endothelial dysfunction; hypothesis-generating for human translation.
In stroke-prone spontaneously hypertensive rats, increased eNOS activation and iNOS-mediated NO bioavailability appear to play a compensatory role for decreased vasorelaxation, though potentially contributing to further endothelial dysfunction.
Wynne et al. (2018) studied Hypertension. Stroke-prone spontaneously hypertensive rat (SHRSP) model vs. Wistar-Kyoto (WKY) controls was evaluated on Mesenteric artery vasorelaxation (response to acetylcholine). Mesenteric arteries from stroke-prone spontaneously hypertensive rats exhibited decreased relaxation responses to acetylcholine compared with Wistar-Kyoto controls, with increased eNOS activation.
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