ROLE OF CEREBROVASCULAR AND CARDIOVASCULAR CO2-REACTIVITY IN THE PATHOGENESIS OF ARTERIAL HYPERTENSION

Abstract

Intense emotions cause arousal of the central nervous system, sympathetic activation, blood pressure (BP) increase and hyperventilation. Continuous negative emotions coming with hyperventilation lead to increase in CO2-chemosensitivity that keeps chronic hypocapnia constant and results in BP dysregulation and stable arterial hypertension (AH). The key mechanism of a hypertensive effect of chronic hyperventilation probably lies in sensitivity changes of CO2-chemoreceptors. Respiratory training with periodic hypercapnia has potential therapeutic effect in HTN by restoring CO2-chemoreceptor sensitivity and increasing antioxidant activity. Hypocapnia violates autoregulation mechanisms. Cerebral blood vessels lose their ability to neutralize BP surges, which negatively affects chemoreceptor-related processes of respiratory and BP regulation. With the HTN progression, cerebrovascular dysregulation occurs depending on the BP level. Moreover, hypocapnia is accompanied by the reduction of intracranial venous tone which can lead to increased intracranial pressure and problems with BP regulation in the brain. The threshold level of cardiovascular CO2-reactivity is normally higher than the threshold level of cerebrovascular CO2-reactivity. The changes in cardiovascular CO2-reactivity occur already in the initial period of HTN. Compared to healthy people, hypertensive patients develop slower BP reaction to hyper/hypocapnia, and hypercapnia induced low BP does not restore to the baseline level that can result from the BP dysregulation. In general, cerebrovascular CO2-reactivity is decreased in HTN patients. However, the cerebrovascular vasodilator function is preserved better than the vasoconstrictor reserve demonstrating that cerebral vessel remodeling in HTN is characterized by luminal narrowing due to the vascular wall hypertrophy.