February 1, 2001Hypertension
Pulse Pressure, Aortic Reactivity, and Endothelium Dysfunction in Old Hypertensive Rats
Key result
In old hypertensive rats, increased KCl reactivity is endothelium independent and influenced by MAP-dependent hypertrophy, whereas increased NE reactivity is endothelium dependent with increased PP.
Population
3- to 78-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR)
Comparison
Assessment of aortic reactivity using organ… vs Wistar-Kyoto rats (WKY) as normotensive controls
Design
Preclinical
Authors
Discussion
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Implication
Distinguishes MAP- from PP-driven vascular reactivity in aged hypertensive rats; leaves open human translation.
Structured PICO
P
Population
3- to 78-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR)
I
Intervention
Assessment of aortic reactivity using organ chambers, invasive blood pressure, carotid diameter, and histomorphometry
C
Comparator
Wistar-Kyoto rats (WKY) as normotensive controls
O
Outcome
Aortic reactivity (maximal developed tension under KCl and norepinephrine), mean arterial pressure (MAP), and pulse pressure (PP)surrogate
The study demonstrates that in aging hypertensive rats, increased pulse pressure is linked to endothelium-dependent alterations in vascular reactivity, whereas mean arterial pressure increases are associated with endothelium-independent hypertrophy.
Cite This Study
Chamiot‐Clerc et al. (2001) studied Hypertension. Spontaneously hypertensive rats (SHR) vs. Wistar-Kyoto rats (WKY) was evaluated on Aortic reactivity (maximal developed tension under KCl and norepinephrine). In old hypertensive rats, increased KCl reactivity is endothelium independent and influenced by MAP-dependent hypertrophy, whereas increased NE reactivity is endothelium dependent with increased PP.