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Pulse pressure, aortic reactivity, and endothelium dysfunction in old hypertensive rats
P Chamiot-Clerc1, J F Renaud, M E Safar
1Medical Research Department, CNRS ESA 8078, Marie Lannelongue Hospital, 92350 Le Plessis-Robinson, France.
Hypertension (Dallas, Tex. : 1979)
|March 7, 2001
Summary
Hypertension in old rats shows increased aortic stiffness. Reactivity to KCl is endothelium-independent, while norepinephrine reactivity is endothelium-dependent, linked to pulse pressure and altered endothelial function.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Hypertension Research
Background:
- Aortic reactivity in aging hypertensive rats remains poorly understood concerning blood pressure phenotypes.
- Investigating the relationship between mean arterial pressure (MAP), pulse pressure (PP), and aortic function is crucial.
Purpose of the Study:
- To examine aortic reactivity in aging spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) in relation to MAP and PP.
- To elucidate the roles of the endothelium and vascular smooth muscle in age-related changes in aortic function.
Main Methods:
- Organ chamber studies and invasive measurements of blood pressure, carotid diameter, and histomorphometry were employed.
- Aortic tension development under KCl and norepinephrine (NE) was assessed with and without endothelium (E).
Main Results:
- SHR exhibited elevated MAP and PP, with a selective PP increase at 78 weeks.
- KCl-induced tension increased linearly with age in SHR, independent of the endothelium.
- NE-induced tension showed age-dependent increases, with endothelial dysfunction observed in SHR beyond 12 weeks.
Conclusions:
- Increased KCl reactivity in old hypertensive rats is endothelium-independent, driven by MAP-dependent hypertrophy and smooth muscle reactivity.
- Enhanced NE reactivity is endothelium-dependent, associated with increased PP, altered endothelial function, and extracellular matrix changes, leading to arterial stiffness.