Aortic pressure pulse amplification in normotensive, hypertensive and aortic calcified rats

Arterial blood pressure (BP) consists of a steady mean arterial pressure (MAP) and a pulsatile pulse pressure (PP). As the pressure wave travels distally from the heart, MAP and diastolic BP remain essentially constant but a gradual and significant increase of systolic BP and PP occurs. The aim of this study was to characterize the amplification of PP (PPA) between the proximal and distal aortic sites in Wistar Kyoto (WKY), spontaneously hypertensive (SHR) and calcified (VDN) rats. Experiments were performed in anaesthetised (Urethane, 1.3 g/kg, ip) WKY, age matched SHR and VDN rats (n6 in each group). Calcification was induced in 8 weeks old WKY with vitamin D3 (300000 IU/kg, im) and 2 doses of nicotine (25 mg/kg, p.o.), one with vitamin D3 injection and the second after 8 hours. Using simultaneous catheterization of proximal and distal aorta with two high fidelity 1.4F catheters, aortic beat-to-beat PPA was recorded over a wide range of BP. MAP was increased and decreased by 30 second infusions of phenylephrine (50 g/min.) and sodium nitroprusside (10 g/min). PPA is defined as the ratio of the PP recorded at the distal sensor to the proximal. PPA-MAP curves were obtained for pressure range of 50 to 160 mmHg. PPA increased up to the anesthetised operating MAP and then decreased thereafter. PPA was reduced in SHR and VDN compared to WKY at all pressure. Maximal PPA was 1.4 for WKY at a MAP of 90 and 1.15 and 1.18 for VDN and SHR for MAP of 96 and 122 respectively. PPA in all three groups showed a biphasic relationship with MAP. Isobaric PPA was reduced for SHR up to 120 mmHg compared to WKY then converged to unity. PPA of VDN was attenuated to that of SHR but did not converge to WKY suggesting intrinsic changes might have occurred in the vascular properties.