The relationship between blood pressure and pain

Abstract

The relationship between pain and hypertension is potentially of great pathophysiological and clinical interest, but is poorly understood. The perception of acute pain initially plays an adaptive role, which results in the prevention of tissue damage. The consequence of ascending nociception is the recruitment of segmental spinal reflexes through the physiological neuronal connections. In proportion to the magnitude and duration of the stimulus, these spinal reflexes cause the activation of the sympathetic nervous system, which increases peripheral resistances, heart rate, and stroke volume. The response also involves the neuroendocrine system, and, in particular, the hypothalamic-pituitary-adrenal axis, in addition to further activation of the sympathetic system by adrenal glands. However, in proportion to an elevation in resting blood pressure, there is a contemporary and progressive reduction in sensitivity to acute pain, which could result in a tendency to restore arousal levels in the presence of painful stimuli. The pathophysiological pattern is significantly different in the setting of chronic pain, in which the adaptive relationship between blood pressure and pain sensitivity is substantially reversed. The connection between acute or chronic pain and cardiovascular changes is supported observationally, but some of this indirect evidence is confirmed by experimental models and human studies. The pain regulatory process and functional interaction between cardiovascular and pain regulatory systems are briefly reviewed. Various data obtained are described, together with their potential clinical implications.

Figure 1

The detection of noxious stimuli requires the activation of peripheral sensory organs and the signal transduction pathways for the conduction to the central nervous system. The transport of the nociceptive information to the higher levels of the central nervous system occurs through multiple and parallel upward projections, which lead the signal from the spinal cord to the centers of the prosencephalon, mesencephalon, and cortex.

Figure 2

The beginning of the pain reaction, elicited by nociceptive stimuli, mainly activates norepinephrine‐ and corticotropin‐releasing hormone by locus coeruleus. The adaptability of the body to environmental changes is specifically modulated in various brain areas by different circuits. The central amygdaloideus nucleus, receiving enteroceptive pathways, is indirectly linked to the brainstem, while the medial one, activated by emotional stimuli, is synaptically linked to the paraventricular medial nucleus by the stria terminalis, the preoptic area, and the anterior hypothalamus. Serotonin and acetylcoline stimulates hypothalamus‐pituitary‐adrenal axis, while nitric oxide and gamma‐aminobutyric acid inhibit corticotrophin and vasopressin release, trough limbic system. Catecholamines and serotonin release are regulated by the levels of cortisol, determining the phenomena of habituation to repeated or new pain stresses.

Figure 3

Neuroanatomy of the descending pathway.

Figure 4

Mechanisms of interaction between control of the cardiovascular system and nociception.