Aortic stiffness is dependent on direction of mean arterial pressure change
It is known that aortic stiffness, as measured by pulse wave velocity (PWV), is dependent on
mean arterial pressure (MAP). It has been anecdotally observed that this relationship
demonstrates a directional dependence; ie, PWV is higher at the same MAP when pressure
is rising than when it is falling. The exact mechanisms responsible for this are not fully
understood. The aim of this study was to quantify this directional dependence in a
normotensive and hypertensive strain of rat. Three, 16 week old Spontaneously …
mean arterial pressure (MAP). It has been anecdotally observed that this relationship
demonstrates a directional dependence; ie, PWV is higher at the same MAP when pressure
is rising than when it is falling. The exact mechanisms responsible for this are not fully
understood. The aim of this study was to quantify this directional dependence in a
normotensive and hypertensive strain of rat. Three, 16 week old Spontaneously …
Abstract
It is known that aortic stiffness, as measured by pulse wave velocity (PWV), is dependent on mean arterial pressure (MAP). It has been anecdotally observed that this relationship demonstrates a directional dependence; ie, PWV is higher at the same MAP when pressure is rising than when it is falling. The exact mechanisms responsible for this are not fully understood. The aim of this study was to quantify this directional dependence in a normotensive and hypertensive strain of rat. Three, 16 week old Spontaneously Hypertensive Rats (SHR) and four, 16 week old Wistar Kyoto rats (WKY) were anaesthetized and two pressure sensors were introduced into the thoracic and abdominal aorta. Pressure was increased with phenylephrine administered intravascular via a bolus injection or an infusion (30μg/kg/min) and allowed to return to baseline. Pressure was decreased in the same manner with sodium nitroprusside. Aortic PWV and thoracic MAP were recorded over the entire pressure range. A maximal directional dependence was observed at MAPs of 70mm Hg and 120mm Hg. The directional dependence was greater in the SHR compared to the WKY rats. It was also greater at higher pressure ranges than at lower pressures. Directional dependence was also more pronounced when pressure-altering drugs were administered in a bolus as opposed to a controlled infusion, indicating that there may be a rate-dependent component; that is, the effect is diminished when the MAP changing stimulus is applied slowly. There is likely an interaction between the mechanical and viscoelastic properties of the arteries which determine the level of directional dependence observed in the PWV-MAP relationship. This information may be useful in understanding altered vascular responses in hypertension and cardiovascular disease.
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