Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform

Abstract

Vayssettes-Courchay C, Ragonnet C, Isabelle M, Verbeuren TJ. Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform. Am J Physiol Heart Circ Physiol 301: H382-H390, 2011. First published May 20, 2011 doi:10.1152/ajpheart.00094.2011.-Large-artery stiffening is a major risk factor in aging and hypertension. Elevated blood pressure (BP) and vascular wall properties participate in arterial stiffening; we aimed to evaluate their respective role by combining echo-tracking and the spontaneously hypertensive rats (SHR) treated with low doses of a nitric oxide synthase inhibitor, shown to have arterial stiffening. Normotensive [Wistar-Kyoto (WKY)], SHR, and SHR treated for 2 wk with N G -nitro-L-arginine methyl ester (SHRLN) were anesthetized; BP and distension (pulsatile displacement) of the aortic walls with the ArtLab echo-tracking device were measured. Stiffness index increased in SHRLN vs. SHR; compliance, distensibility, and the slopes and area of the distension-pressure loop curve decreased. The pulsatile distension and pressure waveforms were strongly altered in SHRLN. Maximal values were decreased and increased, respectively, and the waveform kinetics also differed. Thus the area under the curve adjusted to heart rate (AUC/ms) was calculated. Acute BP reductions were induced by diltiazem in SHR and SHRLN, to levels similar to those of WKY. In SHR, compliance, distensibility, stiffness index, and the ascending slope of the distension-pressure loop reached the values of WKY, whereas they were only partially improved in SHRLN. Aortic distension (maximal value and AUC/ms) and the area of the distension-pressure loop were improved in SHR, but not in SHRLN. These data confirm the aortic stiffening induced by nitric oxide reduction in SHR. They show that the ArtLab system analyzes aortic stiffness in rats, and that the aortic pulsatile distension waveform is a parameter strongly dependent on the vascular wall properties.hypertension; compliance; distensibility; pulse-wave velocity; nitric oxide; spontaneously hypertensive rats ARTERIAL STIFFENING IS A MAJOR cardiovascular risk factor (6,17,26,27) in hypertension, end-stage renal disease, hypercholesterolemia, obesity, and diabetes (9,12,21,28). It is also an age-dependent alteration of the vascular wall (21) that has been defined as an early vascular aging factor (22). Elevated blood pressure, inflammation, endothelial dysfunction, remodeling, and hypertrophy are closely related factors that lead to organ damage and vascular stiffening. In hypertension, the long-term elevation of blood pressure leads to endothelial damage and vascular wall remodeling. It has also been proposed that remodeling may precede the hypertensive state (30). In hypertensive patients, major therapeutic targets to avoid cardiovascular events are decreases in blood pressure and improvement of the vascular wall protection (6, 21). Up until now, it remains difficult in humans and in animals to separate the causal effects of blood pressure eleva...

Chronic Reduction of Nitric Oxide Level in Adult Spontaneously Hypertensive Rats Induces Aortic Stiffness Similar to Old Spontaneously Hypertensive Rats

“…To further complete our observations, we performed an acute decrease in BP in order to better characterize the arterial wall stiffness independently of the BP component. In accordance with a previous study by our research group [34], an acute decrease in BP by a bolus administration of clonidine did not improve aortic isobaric distensibility in SHR/ L -NAME. In contrast a chronic BP reduction by a 2-week treatment with perindopril improves it, demonstrating that transmural pressure per se is not the major factor but that the long-term elevation of BP associated with vascular wall alteration is responsible for the aortic stiffening in SHR/ L -NAME.…”

Delayed Ipsilateral Parenchymal Hemorrhage Following Flow Diversion for the Treatment of Anterior Circulation Aneurysms

“…30 The standard method to measure vessel wall compliance is the echo-tracking system, 31 but no devices exist for intracranial vessels. Devices to measure in vivo vessel wall compliance with optical coherence elastography are under development, 32 as well as noninvasive imagebased computer models.…”

Contraction by Ca2+ Influx via the L-Type Ca2+ Channel Voltage Window in Mouse Aortic Segments is Modulated by Nitric Oxide

“…In the large conduit arteries, L-type Ca 2+ channels are important determinants of their mechanical properties and compliance, which are such that blood pressure and flow are propagated between the heart and arterioles and that thereby pulsatile flow is transformed into steady flow due to the "windkessel" effect (Westerhof et al, 2009). For example, CaBs increase vascular compliance of large elastic vessels and may be of importance for the pathogenesis and prognosis of cardiovascular complications such as atherosclerosis, left ventricular hypertrophy and heart failure (Bellien et al, 2010;Belz, 1995;Essalihi et al, 2007;Safar et al, 1989;Slama et al, 1995;Vayssettes-Courchay et al, 2011). Further evidence for a role of L-type Ca 2+ channels in atherosclerosis was obtained in carotid and femoral VSMCs, where the L-type Ca 2+ channel gene expression differs between atherosclerotic versus non-atherosclerotic regions (Tiwari et al, 2006).…”