Baroreceptor ablation in spontaneously hypertensive rats showed a 43% loss of aortic inhibitory function, indicating hypertension is due to central resetting rather than baroreceptor dysfunction.
The combined and individual carotid sinus and aortic baroreceptor control of sympathetic nerve activity (SNA) and mean arterial pressure (MAP) were studied by direct measurement in groups of spontaneously hypertensive rats (SHR) and normotensive Kyoto Wistar rats (WKY) of 5 to 40 weeks of age. The SHR showed a significantly greater SNA and resultant MAP increase as a function of age compared to that of the WKY rats. Both SHR and WKY rats showed a significant rise in SNA and MAP with ablation of all four major baroreceptors. The proportionate change of SNA and MAP after ablation was greater in the younger SHR than in the younger WKY groups and the change in these decreased as a function of age in the SHR. The reflex inhibition of SNA via baroreceptor stimulation also decreased as a function of age in the SHR, due to a 43% loss of aortic inhibitory function; no significant loss of carotid sinus function was found in either the SHR or WKY. The decrement in aortic function occurred after the rapid phase of blood pressure development; therefore baroreceptor dysfunction cannot be the cause of the high SNA and MAP observed in young SHR. An upward resetting of central sympathetic centers was evaluated via the baroreceptor deafferentation; and it appears that the hyperactive sympathetic nervous system and resultant hypertension in the SHR is due to central resetting of sympathetic centers rather than baroreceptor dysfunction.
Judy et al. (Thu,) conducted a other in Hypertension. Baroreceptor ablation vs. Normotensive Kyoto Wistar rats (WKY) was evaluated on Sympathetic nerve activity (SNA) and mean arterial pressure (MAP). Baroreceptor ablation in spontaneously hypertensive rats showed a 43% loss of aortic inhibitory function, indicating hypertension is due to central resetting rather than baroreceptor dysfunction.