Physiological Mechanisms underlying Blood Pressure related Hypoalgesia

Abstract

Blood pressure hypoalgesia describes the phenomenon that increased blood pressure
causes reduced pain sensation. Pain serves as a warning of actual or potential tissue
damage and is therefore critical to avoid further injury.
Studies in people with high blood pressure, as well as increased risk of high blood
pressure, have shown that perceived pain to wide range of stimuli is diminished in this
population. The mechanism underlying hypertension hypoalgesia is unknown. Three
main theories have been proposed; 1) the baroreceptor hypersensitivity hypothesis, 2)
the sympathetic hyperactivity hypothesis, and 3) the opioid hyposensitivity hypothesis.
This thesis explores the physiological mechanisms underlying blood pressure-related
hypoalgesia. Blood pressure hypoalgesia was shown to be unrelated to blood pressure
reactivity and baroreflex gain in healthy volunteers. Ambulatory blood pressure in the
normal-to-high range showed no association with pain perception or pain thresholds.
However, resting mean arterial pressure showed a negative correlation with activity in
the dorsolateral periaqueductal grey during pain.
In addition to exploring the physiology of blood pressure hypoalgesia, this thesis
investigated whether blood flow related measurements are appropriate for studying
central neural activation by magnetic resonance imaging (MRI) techniques (such as
blood oxygen level dependant (BOLD) signals) in people with high blood pressure.
Brain blood flow at rest has been shown to be lower in hypertensive individuals.
Whether cerebral blood flow is impacted by variations in systemic blood pressure or
central blood volume in people with hypertension versus healthy controls is unclear.
This could have implications in the interpretation BOLD signals in this group. These
studies found no significant difference in the regulation of brain blood flow during a
haemodynamic challenge between hypertensive and normotensive participants.
Therefore BOLD imaging could be used to understand the central nuclei involved in
blood pressure hypoalgesia in hypertensive participants.
It was concluded that blood pressure hypoalgesia is not dependent on absolute blood
pressure or blood pressure reactivity. It is possible that blood pressure hypoalgesia is
related to hypertension risk and/or opioid hyposensitivity. Future work is warranted for
the investigation of the opioid hyposensitivity hypothesis of blood pressure
hypoalgesia.

Date of Award	6 Nov 2018
Original language	English
Awarding Institution	University of Bristol
Supervisor	Jonathan C W Brooks (Supervisor), Emma C J Hart (Supervisor) & Giovanni Biglino (Supervisor)