Abstract
The causes of essential hypertension remain an enigma. Interactions between genetic and external factors are generally recognized to act as aetiological mechanisms that trigger the pathogenesis of high blood pressure. However, the questions of which genes and factors are involved, and when and where such interactions occur, remain unresolved. Emerging evidence indicates that the hypertensive response to pressor stimuli, like many other physiological and behavioural adaptations, can become sensitized to particular stimuli. Studies in animal models show that, similarly to other response systems controlled by the brain, hypertensive response sensitization (HTRS) is mediated by neuroplasticity. The brain circuitry involved in HTRS controls the sympathetic nervous system. This Review outlines evidence supporting the phenomenon of HTRS and describes the range of physiological and psychosocial stressors that can produce a sensitized hypertensive state. Also discussed are the cellular and molecular changes in the brain neural network controlling sympathetic tone involved in long-term storage of information relating to stressors, which could serve to maintain a sensitized state. Finally, this Review concludes with a discussion of why a sensitized hypertensive response might previously have been beneficial and increased biological fitness under some environmental conditions and why today it has become a health-related liability.
Accepted Version (
Free)
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call