[Physiology and methods for studying the baroreceptor reflex].
The baroreflex is of major importance for the moment-to-moment maintenance of arterial pressure particularly during orthostatic stress. Blood pressure increase stimulates the receptors e.g. in the carotid sinuses and the aortic arch, and rapidly increases the receptor discharge rate. Blood pressure decrease induces arrest of impulse transmission to the nucleus of the solitary tract. The impulses are modulated by the nucleus ambiguous, the rostral ventrolateral medulla, the dorsal nucleus of the vagus nerve, parabrachial and paraventricular nuclei and other central structures. Blood pressure increase induces an increase of cardiovagal activity resulting in cardiodeceleration and a decrease of sympathetic peripheral vasoconstrictor outflow. The receptor firing rates show adaptation and resetting to longer lasting blood pressure changes, hysteresis, i.e. firing rates that are higher with rapid blood pressure increase than during the return to baseline pressure. The receptors interact with respiration, chemoreceptor stimulation, central stimuli, exercise and sleep, etc. Baroreceptor function and interaction e.g. with chemoreceptors is compromised in diseases such as diabetic autonomic neuropathy. Guillain-Barré syndrome, arterial hypertension, heart failure and probably in most stroke patients. Fatal complications may result from baroreceptor malfunction. Subtle analysis of the baroreflex is therefore crucial for a refined pathophysiological understanding of these diseases. Pharmacological testing and "neck chamber" negative pressure stimulation of the receptors are as useful as the non-invasive computerized analysis of the interaction of spontaneous blood pressure and heart rate fluctuations.
Hilz
M J
MJ
Neurologische Klinik mit Poliklinik, Friedrich-Alexander-Universität Erlangen-Nürnberg. max.hilz@neuro.med.uni-erlangen.de
Stemper
B
B
Neundörfer
B
B
D001013:Aorta, Thoracic / Q000294:innervation; D001794:Blood Pressure / Q000502:physiology*; D001921:Brain / Q000503:physiopathology; D002346:Carotid Sinus / Q000294:innervation; D006801:Humans; D009434:Neural Pathways / Q000503:physiopathology; D011311:Pressoreceptors / Q000502:physiology*; D012018:Reflex / Q000502:physiology*; D012021:Reflex, Abnormal / Q000502:physiology