Impaired endothelium-mediated cerebrovascular reactivity promotes anxiety and respiration disorders in mice.

ABSTRACT: Carbon dioxide (CO₂), the major product of metabolism, has a strong impact on cerebral blood vessels, a phenomenon known as cerebrovascular reactivity. Several vascular risk factors such as hypertension or diabetes dampen this response, making cerebrovascular reactivity a useful diagnostic marker for incipient vascular pathology, but its functional relevance, if any, is still unclear. Here, we found that GPR4, an endothelial H⁺ receptor, and endothelial Gα_q/11 proteins mediate the CO₂/H⁺ effect on cerebrovascular reactivity in mice. CO₂/H⁺ leads to constriction of vessels in the brainstem area that controls respiration. The consequential washout of CO₂, if cerebrovascular reactivity is impaired, reduces

SUBMITTER: Wenzel J 

PROVIDER: S-EPMC6983400 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature