Key result
Carotid sinus nerve stimulation historically induces bradycardia and systemic hypotension as baroreceptors adapt to hypertension.
Why the study?
The mechanisms underlying the carotid sinus reflex and its role in systemic blood pressure regulation were studied historically but require organized description.
This paper reviews the historical physiological studies elucidating the mechanisms of the carotid sinus reflex, including bradycardia and systemic hypotension.
Historical carotid sinus nerve stimulation effects should not guide practice; leaves open need for modern validation of baroreceptor adaptation.
The first organized study and description of the carotid sinus reflex was made in 1924 by H. E. Hering. ’ He demonstrated two separate cardiovascu-lay rrflrxr<-hra4ycardia and systemic hypotension-by stimulating the cen-tral end of the carotid sinus nerve, by tugging on the common carotid artery, and by stimulating the internal wall of the sinus region with a sound. Cutting the carotid sinus nerve not only abolished these responses, but caused sys-temic hypertension. In 1932, Bronk and Stella3 recorded a discharge of im-pulses from the entire carotid sinus nerve as well as from single end-organs. They demonstrated the tonic activity of the carotid sinus nerve baroreceptors, delineated the range of pressures at which peak activity occurred, and noted the synchronous outburst of impulses during cardiac systole. The fact that the carotid baroreceptors seem to adapt to hypertensive levels has been demonstrated by several workers. 13-15 One found no significant dif-ference between the degree of blood pressure and pulse rate elevation in normotensives and that in hypertensives following procaine block of the
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Stansel et al. (1968) conducted a review in Hypertension. Carotid sinus nerve stimulation was evaluated. Carotid sinus nerve stimulation was historically shown to induce bradycardia and systemic hypotension, with baroreceptors adapting to hypertensive levels.
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