Breathing and blood pressure are functionally linked – think of the biathletes that regulate their breathing to slow heart rate prior to rifle shooting. These effects occur via the brain pathways that generate nervous activity to the heart and blood vessels – the sympathetic nervous system.
During the development of hypertension there is an altered interaction between the neural circuit that generates breathing and the one generating sympathetic nerve activity. A new study from the Department of Physiology at The University of Melbourne and the Faculty of Medicine and Health Sciences at Macquarie University has outlined the brain cell groups responsible for this altered interaction. Interruption of the activity of one group of neurons in this pathway dramatically reduces the development of high blood pressure in a rat model. These neurons represent a target for the development of therapies to stop the development of high blood pressure.
Are some humans at risk of developing high blood pressure due to altered breathing and sympathetic interactions? The study showed that some University-age students who have an elevated blood pressure response to mild exercise, and are known to have increased risk of developing high blood pressure in middle age, also have increased breathing-related regulation of blood pressure at rest.
The new study, funded by grants from the NHMRC and the ARC, was led by Dr Clement Menuet, a McKenzie Fellow at The University of Melbourne, and Prof. Andrew Allen and will be published in Cell Metabolism, a leading journal for metabolic and cardiovascular diseases.