Abstract
Aims: Arterial baroreceptors are located in vessels which are subject to atherosclerotic changes. Using a rabbit model, we investigated effects of atherosclerosis on arterial baroreceptors, arterial baroreflex regulation and control of Mean Arterial Pressure (MAP).
Methods and results: Seven-week-old male New Zealand White rabbits were placed on an atherogenic diet for 14 weeks (treatment). Treatment produced significant atherosclerosis along the aorta, but spared the carotid bifurcation. Treated animals had higher MAP: conscious–(treated: 80.1 [77.3, 82.9] versus control: 70.9 [69.9, 71.9] mmHg; N = 7 and 9 respectively; p = < 0.001) (mean [90% confidence interval]), anaesthetized–(treated: 99.9 [97.2, 102.7] versus control: 95.6 [93.5, 97.7] mmHg, N = 24 for each group; p = 0.050). In anaesthetized animals Pulse Wave Velocity (PWV) along the aorta was higher in treated animals (5.64 [5.54, 5.74] versus 5.07 [4.98, 5.16] m/s in control, N = 24 for each group; p < 0.0001). MAP was ramped (from 40 to 140 mmHg) using inflatable cuffs around the descending aorta and posterior vena cava. Treatment did not affect the activity of individual A-fibre baroreceptors in the ADN. Multifibre records of activity in the left Aortic Depressor Nerve (ADN) and left Carotid Sinus Nerve (CSN), showed that treatment reduced C-fibre baroreceptor activity in the ADN; there was ~16.5% less integrated activity at MAP >100 mmHg in treated animals (4650 [4174, 4988] versus 5570 [5220, 5919] au in control; N = 22 and 20, respectively; p < 0.001). Treatment had no effect on multifibre recordings from the CSN.
In conscious animals, baroreflex curves describing control of Renal Sympathetic Activity (RSNA) were obtained using i.v. phenylephrine and nitroprusside to modify MAP. Treatment shifted the mid-point of the curve to a higher MAP (72.4 [69.9, 74.8] versus 63.6 [61.3, 65.8] mmHg in control; N = 5 and 8, respectively; p = 0.02. In anaesthetized animals, baroreflex curves for RSNA were obtained using inflatable cuffs to control MAP. When input from the CSN was kept low and steady by common carotid artery occlusion, a high level of MAP was unable to fully inhibit RSNA (12.5 [8.4, 16.6] and 3.9 ([2.6, 5.2] n.u. at saturation in 5 treated and 7 control animals, respectively; p = 0.01).
Conclusion: The loss of aortic C-fibre baroreceptor activity that occurs in this model of atherosclerosis may reset MAP to a higher value, since C-fibre input is likely a controller of MAP.
![Integrated baroreceptor activity during a pressure ramp. Lines show the normalised mean activity from treated (dashed) and control (solid) animals. Representative error bars show 1SD.
(A.) Mean of normalised integrated CSN activity from 10 treated and 10 control animals. (B) Mean of normalised integrated ADN activity from 22 treated and 20 control animals. The mean area under the curve at pressures above 90 mmHg was smaller in treated than in control animals (4650 [4174, 4988] versus 5570 [5220, 5919] au; p < 0.001, single-tailed t-test.](https://www.igminresearch.com/articles/figures/igmin340/igmin340.g001.png)
