Reflex vascular responses from aortic, carotid and coronary baroreceptors

1. Many studies which have examined reflexes from the left ventricle have failed adequately to localise the pressure stimulus to that area, and have caused simultaneous changes in coronary pressure. Recent studies demonstrate that localized changes in pressure, over a physiological range, to the coronary arteries results in reflex vascular responses. The coronary arteries thus function as baroreceptors. However, there has been no study to compare the characteristics of coronary baroreceptors with those of aortic arch and carotid sinus receptors. This study was therefore designed to compare and contrast these three baroreceptor regions.
2. The experiments described in this thesis were all performed in anaesthetized dogs attached to perfusion circuits. This allowed independent control of pressures perfusing the coronary arteries, aortic arch and carotid sinuses. A cardiopulmonary bypass and an oxygenator incorporated into some of the circuits allowed control of the pulsatility of the pressures applied to the coronary arteries. Reflex responses were assessed from changes in perfusion pressure to the systemic and hind limb circulations and from changes in sympathetic efferent nerve discharge recorded from renal and lumbar nerves.
3. The time courses of the vascular responses to loading and unloading coronary baroreceptors were investigated and compared with responses from aortic arch and carotid sinus baroreceptors. All three baroreceptor groups when stimulated initiated rapid reflex vasodilatation Coronary baroreceptor unloading resulted in vasoconstriction that was significantly slower than that from either aortic arch or carotid sinus baroreceptors. This effect was not altered by increasing the duration at high coronary pressure from 30 s to 8 minutes or by making the stimulus pressure non-pulsatile. The time course of the responses from aortic and carotid baroreceptors were rapid and not different from each other.
4. A further series of experiments examined the mechanism of the slow coronary induced vasoconstriction. Electrophysiological recordings of sympathetic efferent nerves showed that they responded rapidly to increases in coronary pressure but slowly to decreases, thus mirroring the vascular response. Sympathetic efferent nerve responses to changes in carotid and aortic pressure were rapid.
5. Further experiments compared the responses of each baroreceptor group to non- pulsatile and pulsatile stimuli and their operating ranges. There was no difference between the response curves to non-pulsatile and pulsatile stimulation of coronary baroreceptors. Stimulation of carotid receptors with pulsatile pressures shifted the response curve to lower carotid pressures. Pulsatile aortic pressures induced greater vasodilatation over the mid-range of the baroreceptor response curve compared to non-pulsatile pressures. The threshold for responses from coronary baroreceptors was extremely low with responses obtained at the lowest pressures tested. The operating range of the coronary baroreceptors was over significantly lower pressures than for aortic or carotid baroreceptors, which both had similar operating ranges.
6. These results demonstrate that coronary baroreceptors operate mainly in hypotensive situations initiating a slow vasoconstriction to unloading and were active at extremely low pressures. They are insensitive to changes in pulse pressure whereas both aortic and carotid baroreceptors were sensitive.